外源性硫化氢对创伤失血性休克大鼠保护作用的研究
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摘要
创伤失血性休克(traumatic hemorrhagic shock, THS)是指机体遭受严重创伤后引起的以微循环障碍为主要特征的急性循环功能不全的休克类型,常伴随多器官损伤。创伤失血性休克早期,由于血管内有效血容量不足,组织缺血缺氧性坏死、细胞凋亡,引起大量伤害性化学介质释放;后期液体复苏时缺血再灌注(ischemia-reperfusion, I/R)损伤又增加耗氧,增强氧化应激反应,激发炎症因子爆发,血管被阻塞出现“无复流”现象,导致细胞摄取氧功能障碍,进一步造成器官再灌注损伤,降低复苏后存活率。因此,如何维持组织细胞“氧供-氧耗”平衡,减少缺血再灌注损伤成为救治创伤失血性休克的关键。
硫化氢(hydrogen sulfide,H2S)作为第三类气体信号分子,已被证实广泛参与了神经系统、心血管系统、呼吸系统、消化系统、氧化应激、细胞代谢及炎症反应等众多病理生理调节过程。研究发现,H2S具有保护重要器官抵御缺血再灌注损伤、提高机体抗氧化应激性损伤能力、减轻炎症反应的作用,并具有明显的代谢抑制效应。但H2S对于创伤失血性休克是否同样具有保护作用至今仍未见报道。
本研究利用大鼠创伤失血性休克模型,通过复苏初期给予外源性硫化氢后,观察模型血流动力学、血气分析指标、重要器官功能及观察病理形态学改变和复苏成功率及存活率的变化,以评价外源性H2S对创伤失血性休克的作用并初步探讨其可能的机制,为创伤失血休克救治提供新思路和方法。
目的
利用大鼠创伤失血性休克模型观察外源性硫化氢对创伤失血性休克损伤的保护作用并初步探讨其可能的作用机理,为创伤失血性休克的救治提供新思路。
方法
1、选择健康清洁级成年SD大鼠48只,雄性,220g-250g,随机分为三组,每组16只:假手术组(Sham组),对照组(Vehicle组),NaHS处理组(NaHS组)。采用创伤失血性休克模型,经3%戊巴比妥麻醉后(40 mg/kg ip),于大鼠腹正中切口5cm然后缝合造成软组织创伤;经右侧股动脉插入聚乙烯导管以备放血,分离右侧股静脉插管以备输液,分离左侧股动脉插管连接压力转换器测量平均动脉压(mean arterial pressure, MAP)及心率(heart rate, HR)。所有切口用利多卡因浸润阻滞,除Sham组外,各组均在10min内迅速放血使MAP降至35-40mmHg;若血压不能维持需补充Ringer’s液,此时为最大放血量(maximal bleed-out, MBO),放血量为大鼠总体血容量的60%,(大鼠总血容量为体重的6%)。MBO后,回输40%MBO容量的Ringer’s液以维持血压在35-40mmHg约90mi(n出血后开始),然后以4倍MBO容量的Ringer’s液在60min内进行复苏,复苏后缝合所有伤口。Sham组完成所有手术操作,但不进行放血和复苏;Vehicle组放血后Ringer’s液复苏前,腹腔注射与NaHS组等容量的生理盐水;NaHS组在复苏前给与腹腔注射28μmol/kg NaHS。复苏后的大鼠拔除所有插管,结扎血管,丝线缝合伤口后放回笼子自由进食饮水观察。
2、术中持续监测各组平均动脉压MAP、HR,复苏后2h检测左室压(left ventricular pressure,LVP)、左心室压力最大上升速率(positive first derivatives of pressure.+dp/dtmax)和左心室压力最大下降速率(negative first derivatives of pressure ,-dp/dtmax),动脉血气分析等指标变化。
3、检测各组大鼠肝功转氨酶及肾功能指标变化。
4、检测肺系数与肺湿/干重比等指标变化,并观察肺组织损伤(IQA)的程度。
5、监测各组大鼠即刻复苏成活率、复苏后6h、24h存活率的变化。
6、测定血浆中H2S、MDA(malondialdehyde)、SOD(superoxide dismutase)、MPO(myeloperoxidase)的变化,观察硫化氢对氧化应激及炎症反应作用。
7、制备大鼠心、肺、肝和肾组织切片行HE染色,观察创伤失血性休克复苏后器官病理形态学的变化。
结果
1、与Sham组相比,Vehicle组复苏后MAP、HR、LVP、+dp/dtmax、-dp/dtmax均明显降低(P<0.05),pH、PaO2值及BE值降低(P<0.05)。与Vehicle组相比,NaHS组MAP、LVP、+dp/dtmax、-dp/dtmax有明显升高(P<0.05),血气指标pH、PaO2值及BE值升高(P<0.05)。
2、Vehicle组在复苏后,肝肾功能指标AST(aspartate aminotransferase)、ALT(alanine aminotransferase)、BUN(blood urea nitrogen)、SCr(serum creatinine)升高(P<0.05)。给予NaHS处理后,上述肝肾功能指标有所降低(P<0.05)。
3、复苏后,Vehicle组及NaHS组肺系数、肺组织湿/干重比及肺损伤指数(IQA)升高(P<0.05),但NaHS组较Vehicle组肺系数、肺湿/干重比减少,肺损伤指数(IQA)降低(P<0.05),提示肺组织水肿减轻、损伤减小。
4、较Vehicle组,NaHS组复苏后24h存活率明显提高(P<0.05)。
5、Vehicle组复苏后,血浆中MDA、MPO增加,SOD活性及血浆H2S浓度降低(P<0.05);与Vehicle组相比,NaHS组血浆中MDA、MPO明显降低,SOD活性及血浆H2S浓度增加(P<0.05)。
6、较Vehicle组,NaHS组在光镜下心、肝、肾组织病理学形态有明显改善。
结论
1、外源性硫化氢对创伤失血性休克大鼠具有保护作用,能够改善复苏后血流动力学参数、增强心脏舒缩功能,改善酸中毒状态,提高液体复苏后24h存活率。
2、外源性硫化氢能够减轻创伤失血性休克复苏后肺组织水肿,提高肝肾功能,改善心、肺、肝、肾组织病理形态。
3、外源性硫化氢对创伤失血性休克大鼠保护作用的机制可能与硫化氢具有的提高机体抗氧化应激反应能力有关。
Traumatic hemorrhagic shock (THS) is a type of shock caused by severe trauma with acute circulatory insufficiency. THS is accompanied with the hypovolemia, hypoxemia,apotosis and microcirculatory disturbance, releasing abundant toxic chemical mediators. Resuscitation will also cause ischemia- reperfusion (I/R) damages which will increase the consumption of oxygen,enhance lipid oxidative stress response, stimulate inflammatory cytokines, resulting in dysfunction of cellular oxygen uptake and aggravating tissue damage. It has been reported that treament of reducing oxidative stress damage and inhibiting the outbreak of inflammatory cytokines make sense in the remedy of trauma-hemorrhagic shock.
H2S is proved to be extensively involved in many pathophysiological processes of the nervous system, cardiovascular system, respiratory system, digestive system, oxidative stress, cell metabolism, and inflammatory responses. Studies found that H2S can protect vital organs against ischemia-reperfusion injuries, improve the defense against oxidative stress injury, reduce the activation of inflammation, and has significant inhibitory effect on metabolism. However, the effect of H2S on traumatic hemorrhagic shock is still not reported yet.
In this study, traumatic hemorrhagic shock model of rats was used to observe the alterations in hemodynamics, cardiac function, tissue injuries, blood gas analysis parameters, and survive rates when giving the exogenous hydrogen sulfide at the beginning of resuscitation. By evaluating the clinical effects of exogenous H2S on traumatic-hemorrhagic shock, we explored the possible mechanisms and expected to provide a new way for the treatments of traumatic hemorrhagic shock.
The protective effects of exogenous hydrogen sulfide against trauma-hemorrhagical shock in rats
Object
To invest the protective effects of exogenous hydrogen sulfide on traumatic hemorrhagic shock in rats.
Methods
1. Forty-eight male Sprague-Dawely rats were divided into 3 groups randomly as follows: (1) Sham group (n=16); (2) Vehicle group (n=16); (3) NaHS group (n=16). Sham-operated rats underwent all the surgical procedures, except neither hemorrhage nor resuscitation. The rats were given the same volume of vehicle or NaHS solution (28μmol/kg) intraperitoneally at the onset of of the resuscitation in group (2) and (3) respectively. After overnight fast with a free access to water, rats were anesthetized with 3% pentobarbital sodium intraperitoneally (40mg/kg). Trauma hemorrhage and resuscitation model was carried out. Briefly, a 5-cm midline laparotomy was performed to make a soft tissue trauma. The abdominal wound was then closed in two layers with sutures. Polyethylene catheters were put in both femoral arteries and the right femoral vein. The incision sites were then closed. The hemodynamic parameters were measured via one of the arteries using a blood pressure analyzer.Then blood was then withdrawn rapidly to a mean arterial pressure (MAP) of 35–40 mmHg in 10 min through the other artery until the animals could no longer maintain MAP of 35–40 mmHg unless some Ringer lactate solution (RL) was administered. This time and volume were recorded as maximal bleed out (MBO). After the MBO, hypotension was maintained between 35 and 40 mmHg by giving 40% of the MBO volume of RL (about 90 min since the beginning of bleeding). The blood withdrawn was about 60% the same as the total volume (6% of the body weight). The animals were then resuscitated with four times the volume of MBO with RL over 60 minutes in vein. After resuscitation, all the catheters were removed and all wounds were closed with sutures. All the incisions were flushed with lidocaine in order to inhibit pain. At the end of whole procedure, rats was then put in a solo cage with food and water ad libitum.
2. Rats were sacrificed 2 hours after resuscitation, and monitored artery mean blood pressure (MAP), heart rate(HR), left ventricular pressure (LVP), positive (+dp/dtmax) and negative (-dp/dtmax) first derivatives of left ventricle pressure. Meanwhile, blood samples were taken to determine the blood gas analysis.
3. The serum samples were then analyzed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and serum creatinine (SCr).
4. W/D ratio and IQA of lung tissue were messured to estimate the edema as well as the injury dgree of pulmonary alveoli.
5. The changes of H2S, malondialdehyde (MDA), myeloperoxidase (MPO) level and superoxide dismutase (SOD) activity were determined after taking serum samples.
6 .The rats were also monitored the variances of survive rates immediaterly and 6h, 24h after resuscitation.
7. Histopathological changes of heart, lung, liver and kidney were observed under light microscope at 2 hours after resuscitation among groups.
Results
1. Compared with sham group, MAP, HR, LVP, +dp/dtmax and -dp/dtmax decreased largely in vehicle group (P<0.05). Compared with vehicle group, NaHS displayed a rise in MAP, LVP, +dP/dtmax and -dP/dtmax (P<0.05).
2. Compared with sham group, pH、PaO2 and BE decreased in vehicle group(P<0.05). Compared with vehicle group, NaHS displayed a rise in pH、PaO2 and BE (P<0.05).
3. NaHS showed a reverse against the raising AST, ALT, BUN and SC(rserum creatinine)compared with the vehicle group after T-H(P<0.05).
4. In the vehicle group, the W/D ratio of lung tissue and IQA increased compared with sham group (P<0.05).But compared with vehicle group, the W/D ratio and IQA in NaHS group decreased largely (P<0.05).
5. NaHS also significantly reversed the high mortality caused by T-H after 24 hours.
6. The NaHS-treated group showed a remarkable decreasing in MDA and MPO levels in plasma as well as a rise in SOD activity compared with those in vehicle-treated group.
7. The histopathological analysis indicated conservation of morphous in heart, liver and kidney in NaHS.group.
Conclusions
1. NaHS attenuated the depression of cardiac function, promoted the stability of hemodynamic parameters and reversed the acidosis, enhancing survival rate 24 hours after trauma hemorrhage and resuscitation.
2. NaHS decreases edema of lung tissue and pulmonary alveoli. NaHS postconditioning also promoted the restoration of hepatic and renal functions.
3. Mechanisms for protective effects of NaHS may be associated with the antioxidative damage of hydrogen sulfide on T-H and resuscitation.
硫化氢(hydrogen sulfide,H2S)作为第三类气体信号分子,已被证实广泛参与了神经系统、心血管系统、呼吸系统、消化系统、氧化应激、细胞代谢及炎症反应等众多病理生理调节过程。研究发现,H2S具有保护重要器官抵御缺血再灌注损伤、提高机体抗氧化应激性损伤能力、减轻炎症反应的作用,并具有明显的代谢抑制效应。但H2S对于创伤失血性休克是否同样具有保护作用至今仍未见报道。
本研究利用大鼠创伤失血性休克模型,通过复苏初期给予外源性硫化氢后,观察模型血流动力学、血气分析指标、重要器官功能及观察病理形态学改变和复苏成功率及存活率的变化,以评价外源性H2S对创伤失血性休克的作用并初步探讨其可能的机制,为创伤失血休克救治提供新思路和方法。
目的
利用大鼠创伤失血性休克模型观察外源性硫化氢对创伤失血性休克损伤的保护作用并初步探讨其可能的作用机理,为创伤失血性休克的救治提供新思路。
方法
1、选择健康清洁级成年SD大鼠48只,雄性,220g-250g,随机分为三组,每组16只:假手术组(Sham组),对照组(Vehicle组),NaHS处理组(NaHS组)。采用创伤失血性休克模型,经3%戊巴比妥麻醉后(40 mg/kg ip),于大鼠腹正中切口5cm然后缝合造成软组织创伤;经右侧股动脉插入聚乙烯导管以备放血,分离右侧股静脉插管以备输液,分离左侧股动脉插管连接压力转换器测量平均动脉压(mean arterial pressure, MAP)及心率(heart rate, HR)。所有切口用利多卡因浸润阻滞,除Sham组外,各组均在10min内迅速放血使MAP降至35-40mmHg;若血压不能维持需补充Ringer’s液,此时为最大放血量(maximal bleed-out, MBO),放血量为大鼠总体血容量的60%,(大鼠总血容量为体重的6%)。MBO后,回输40%MBO容量的Ringer’s液以维持血压在35-40mmHg约90mi(n出血后开始),然后以4倍MBO容量的Ringer’s液在60min内进行复苏,复苏后缝合所有伤口。Sham组完成所有手术操作,但不进行放血和复苏;Vehicle组放血后Ringer’s液复苏前,腹腔注射与NaHS组等容量的生理盐水;NaHS组在复苏前给与腹腔注射28μmol/kg NaHS。复苏后的大鼠拔除所有插管,结扎血管,丝线缝合伤口后放回笼子自由进食饮水观察。
2、术中持续监测各组平均动脉压MAP、HR,复苏后2h检测左室压(left ventricular pressure,LVP)、左心室压力最大上升速率(positive first derivatives of pressure.+dp/dtmax)和左心室压力最大下降速率(negative first derivatives of pressure ,-dp/dtmax),动脉血气分析等指标变化。
3、检测各组大鼠肝功转氨酶及肾功能指标变化。
4、检测肺系数与肺湿/干重比等指标变化,并观察肺组织损伤(IQA)的程度。
5、监测各组大鼠即刻复苏成活率、复苏后6h、24h存活率的变化。
6、测定血浆中H2S、MDA(malondialdehyde)、SOD(superoxide dismutase)、MPO(myeloperoxidase)的变化,观察硫化氢对氧化应激及炎症反应作用。
7、制备大鼠心、肺、肝和肾组织切片行HE染色,观察创伤失血性休克复苏后器官病理形态学的变化。
结果
1、与Sham组相比,Vehicle组复苏后MAP、HR、LVP、+dp/dtmax、-dp/dtmax均明显降低(P<0.05),pH、PaO2值及BE值降低(P<0.05)。与Vehicle组相比,NaHS组MAP、LVP、+dp/dtmax、-dp/dtmax有明显升高(P<0.05),血气指标pH、PaO2值及BE值升高(P<0.05)。
2、Vehicle组在复苏后,肝肾功能指标AST(aspartate aminotransferase)、ALT(alanine aminotransferase)、BUN(blood urea nitrogen)、SCr(serum creatinine)升高(P<0.05)。给予NaHS处理后,上述肝肾功能指标有所降低(P<0.05)。
3、复苏后,Vehicle组及NaHS组肺系数、肺组织湿/干重比及肺损伤指数(IQA)升高(P<0.05),但NaHS组较Vehicle组肺系数、肺湿/干重比减少,肺损伤指数(IQA)降低(P<0.05),提示肺组织水肿减轻、损伤减小。
4、较Vehicle组,NaHS组复苏后24h存活率明显提高(P<0.05)。
5、Vehicle组复苏后,血浆中MDA、MPO增加,SOD活性及血浆H2S浓度降低(P<0.05);与Vehicle组相比,NaHS组血浆中MDA、MPO明显降低,SOD活性及血浆H2S浓度增加(P<0.05)。
6、较Vehicle组,NaHS组在光镜下心、肝、肾组织病理学形态有明显改善。
结论
1、外源性硫化氢对创伤失血性休克大鼠具有保护作用,能够改善复苏后血流动力学参数、增强心脏舒缩功能,改善酸中毒状态,提高液体复苏后24h存活率。
2、外源性硫化氢能够减轻创伤失血性休克复苏后肺组织水肿,提高肝肾功能,改善心、肺、肝、肾组织病理形态。
3、外源性硫化氢对创伤失血性休克大鼠保护作用的机制可能与硫化氢具有的提高机体抗氧化应激反应能力有关。
Traumatic hemorrhagic shock (THS) is a type of shock caused by severe trauma with acute circulatory insufficiency. THS is accompanied with the hypovolemia, hypoxemia,apotosis and microcirculatory disturbance, releasing abundant toxic chemical mediators. Resuscitation will also cause ischemia- reperfusion (I/R) damages which will increase the consumption of oxygen,enhance lipid oxidative stress response, stimulate inflammatory cytokines, resulting in dysfunction of cellular oxygen uptake and aggravating tissue damage. It has been reported that treament of reducing oxidative stress damage and inhibiting the outbreak of inflammatory cytokines make sense in the remedy of trauma-hemorrhagic shock.
H2S is proved to be extensively involved in many pathophysiological processes of the nervous system, cardiovascular system, respiratory system, digestive system, oxidative stress, cell metabolism, and inflammatory responses. Studies found that H2S can protect vital organs against ischemia-reperfusion injuries, improve the defense against oxidative stress injury, reduce the activation of inflammation, and has significant inhibitory effect on metabolism. However, the effect of H2S on traumatic hemorrhagic shock is still not reported yet.
In this study, traumatic hemorrhagic shock model of rats was used to observe the alterations in hemodynamics, cardiac function, tissue injuries, blood gas analysis parameters, and survive rates when giving the exogenous hydrogen sulfide at the beginning of resuscitation. By evaluating the clinical effects of exogenous H2S on traumatic-hemorrhagic shock, we explored the possible mechanisms and expected to provide a new way for the treatments of traumatic hemorrhagic shock.
The protective effects of exogenous hydrogen sulfide against trauma-hemorrhagical shock in rats
Object
To invest the protective effects of exogenous hydrogen sulfide on traumatic hemorrhagic shock in rats.
Methods
1. Forty-eight male Sprague-Dawely rats were divided into 3 groups randomly as follows: (1) Sham group (n=16); (2) Vehicle group (n=16); (3) NaHS group (n=16). Sham-operated rats underwent all the surgical procedures, except neither hemorrhage nor resuscitation. The rats were given the same volume of vehicle or NaHS solution (28μmol/kg) intraperitoneally at the onset of of the resuscitation in group (2) and (3) respectively. After overnight fast with a free access to water, rats were anesthetized with 3% pentobarbital sodium intraperitoneally (40mg/kg). Trauma hemorrhage and resuscitation model was carried out. Briefly, a 5-cm midline laparotomy was performed to make a soft tissue trauma. The abdominal wound was then closed in two layers with sutures. Polyethylene catheters were put in both femoral arteries and the right femoral vein. The incision sites were then closed. The hemodynamic parameters were measured via one of the arteries using a blood pressure analyzer.Then blood was then withdrawn rapidly to a mean arterial pressure (MAP) of 35–40 mmHg in 10 min through the other artery until the animals could no longer maintain MAP of 35–40 mmHg unless some Ringer lactate solution (RL) was administered. This time and volume were recorded as maximal bleed out (MBO). After the MBO, hypotension was maintained between 35 and 40 mmHg by giving 40% of the MBO volume of RL (about 90 min since the beginning of bleeding). The blood withdrawn was about 60% the same as the total volume (6% of the body weight). The animals were then resuscitated with four times the volume of MBO with RL over 60 minutes in vein. After resuscitation, all the catheters were removed and all wounds were closed with sutures. All the incisions were flushed with lidocaine in order to inhibit pain. At the end of whole procedure, rats was then put in a solo cage with food and water ad libitum.
2. Rats were sacrificed 2 hours after resuscitation, and monitored artery mean blood pressure (MAP), heart rate(HR), left ventricular pressure (LVP), positive (+dp/dtmax) and negative (-dp/dtmax) first derivatives of left ventricle pressure. Meanwhile, blood samples were taken to determine the blood gas analysis.
3. The serum samples were then analyzed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and serum creatinine (SCr).
4. W/D ratio and IQA of lung tissue were messured to estimate the edema as well as the injury dgree of pulmonary alveoli.
5. The changes of H2S, malondialdehyde (MDA), myeloperoxidase (MPO) level and superoxide dismutase (SOD) activity were determined after taking serum samples.
6 .The rats were also monitored the variances of survive rates immediaterly and 6h, 24h after resuscitation.
7. Histopathological changes of heart, lung, liver and kidney were observed under light microscope at 2 hours after resuscitation among groups.
Results
1. Compared with sham group, MAP, HR, LVP, +dp/dtmax and -dp/dtmax decreased largely in vehicle group (P<0.05). Compared with vehicle group, NaHS displayed a rise in MAP, LVP, +dP/dtmax and -dP/dtmax (P<0.05).
2. Compared with sham group, pH、PaO2 and BE decreased in vehicle group(P<0.05). Compared with vehicle group, NaHS displayed a rise in pH、PaO2 and BE (P<0.05).
3. NaHS showed a reverse against the raising AST, ALT, BUN and SC(rserum creatinine)compared with the vehicle group after T-H(P<0.05).
4. In the vehicle group, the W/D ratio of lung tissue and IQA increased compared with sham group (P<0.05).But compared with vehicle group, the W/D ratio and IQA in NaHS group decreased largely (P<0.05).
5. NaHS also significantly reversed the high mortality caused by T-H after 24 hours.
6. The NaHS-treated group showed a remarkable decreasing in MDA and MPO levels in plasma as well as a rise in SOD activity compared with those in vehicle-treated group.
7. The histopathological analysis indicated conservation of morphous in heart, liver and kidney in NaHS.group.
Conclusions
1. NaHS attenuated the depression of cardiac function, promoted the stability of hemodynamic parameters and reversed the acidosis, enhancing survival rate 24 hours after trauma hemorrhage and resuscitation.
2. NaHS decreases edema of lung tissue and pulmonary alveoli. NaHS postconditioning also promoted the restoration of hepatic and renal functions.
3. Mechanisms for protective effects of NaHS may be associated with the antioxidative damage of hydrogen sulfide on T-H and resuscitation.
引文
[1] Guidotti T. L. Hydrogen sulphide. Occup Med, 1996, 46(5): 67-371.
[2] Beauchamp RO, Bus JS, Popp JA, Boreiko CJ, Goldberg L. A critical review of the literature on hydrogen sulfide toxicity. CRC Crit Rev Toxicol, 1984, 13: 25-97.
[3] Reiffenstein RJ, Hulbert WC, Roth SH. Toxicology of hydrogen sulfide. Annu Rev Pharmacol Toxicol, 1992, 32: 109-134.
[4] Partlo LA, Sainsbury RS, Roth SH. Effects of repeated hydrogen sulphide (H2S) exposure on learning and memory in the adult rat. Neurotoxicology, 2001, 22(2): 177- 189.
[5] Moore PK, Bhatia M, Moochhala S. Hydrogen sulfide: from the smell of the past to the mediator of the future? Trends Pharmacol Sci, 2003, 24(12): 609- 611.
[6] Abe K, Kimura H. The possible role of hydrogen sulfide as an endogenous neuromodulator. J Neurosci, 1996, 16(3): 1066-1071.
[7] Richardson CJ, Magee EA, Cummings JH. A new method for the determination of sulphide in gastrointestinal contents and whole blood by microdistillation and ion chromatography. Clin Chim Acta, 2000, 293 (1-2): 115– 125.
[8] Stipanuk MH, Beck PW. Characterization of the enzymatic capacity for cysteine desulphhydration in liver and kidney of the rat. Biochem J, 1982, 206 (2): 267–277.
[9] Doeller JE, Isbell TS, Benavides G, Koenitzer J, Patel H, Patel RP, Lancaster JR Jr, Darley-Usmar VM, Kraus DW. Polarographic measurement ofhydrogen sulfide production and consumption by mammalian tissues. Anal Biochem, 2005, 341: 40–51.
[10] Eto K, Kimura H. The production of hydrogen sulfide is regulated by testosterone and S-adenosyl-L-methionine in mouse brain. J Neurochem, 2002, 83 (1): 80 - 86.
[11] Banerjee R, Zou CG. Redox regulation and reaction mechanism of human cystathionine-beta-synthase: a PLP -dependent hemesensor protein. Arch Biochem Biophys, 2005, 433:144-156.
[12] Puranik M, Weeks CL, Lahaye D, Kabil O, Taoka S, Nielsen SB, Groves JT, Banerjee R, Spiro TG.. Dynamics of carbon monoxide binding to cystathionine-β-synthase. J Biol Chem, 2006, 281: 13433–13438.
[13] Taoka S, Banerjee R. Characterization of NO binding to human cystathionine-β-synthase: possible implications of the effects of CO and NO binding to the human enzyme.J Inorg Biochem, 2001, 87: 245–251.
[14] Taoka S, Green EL, Loehr TM, Banerjee R. Mercuric chloride-induced spin or ligation state changes in ferric or ferrous human cystathionine beta-synthase inhibit enzyme activity. J Inorg Biochem, 2001, 87 (4): 253 - 259.
[15] Jacobs RL, Stead LM, Brosnan ME. Hyperglucagonemia in rats results in decreased plasma homocysteine and increased flur through the trans-sulfuration pathway in liver. J Biol Chem, 2001, 276 (47): 43740 -43747.
[16] Dicker BA, Fonseca VA, Fink LM, Kern PA. The effect of glucose and insulin on the activity of methylene tetrahydrofolate reductase and cystathionine-beta-synthase: Studies in hepatocytes. Atherosclerosis, 2001,158 (2): 297 - 301.
[17] Fiorucci S, Distrutti, E, Cirino, G. Wallace, JL. The emerging roles ofhydrogen sulfide in the gastrointestinal tract and liver. Gastroenterology, 2006, 131: 259–271.
[18] Zhao W, Ndisang JF, Wang R. Modulation of endogenous production of H2S in rat tissues. Can J Physiol Pharmacol, 2003, 81: 848–853.
[19] Furne J, Springfield J, Koenig T, DeMaster E, Levitt MD. Oxidation of hydrogen sulfide and methanethiol to thiosulfate by rat tissues: a specialized function ofthe colonic mucosa. Biochem Pharmacol, 2001, 62(2): 255-259.
[20] Kimura H. Hydrogen sulfide induces cyclic AMP and modulates the NMDA receptor. Biochem Biophys Res Commun, 2000, 267: 129–133.
[21] Nagai Y, Tsugane M, Oka J, Kimura H. Hydrogen sulfide induces calcium waves in astrocytes. FASEB J, 2004, 18: 557–559.
[22] Lee SW, Hu YS, Hu LF, Lu Q, Dawe GS, Moore PK, Wong PT. Hydrogen sulphide regulates calcium homeostasis in microglial cells. Glia, 2006, 54: 116–124.
[23] Yuka Kimura, Hideo Kimura. Hydrogen sulfide protects neurons from oxidative stress. Faseb J, 2004, 18: 1165–1167.
[24] Whiteman M, Cheung NS, Zhu YZ, Chu SH, Siau J L, Wong BS, Armstrong JS, Moore PK. Hydrogen sulphide: a novel inhibitor of hypochlorous acid-mediated oxidative damage in the brain? Biochem. Biophys. Res Commun, 2005, 326: 794–798.
[25] Ming Lu, Li-Fang Hu, Gang Hu, Jin-Song Bian. Hydrogen sulfide protects astrocytes against H2O2-induced neural injury via enhancing glutamate uptake. Free Radical Biology & Medicine, 2008, 45: 1705–1713.
[26] Eto K, Asada T, Arima K, Makifuchi T, Kimura H. Brain hydrogen sulfide is severely decreased in Alzheimer’s disease. Biochem Biophys Res Commun, 2002, 293: 1485–1488.
[27] M Whiteman, NS Cheung, YZ Zhu, SH Chu, JL Siau, BS Wong, JSArmstrong, PK Moore. Hydrogen sulphide: a novel inhibitor of hypochlorous acid-mediated oxidative damage in the brain? Biochem Biophys Res Commun, 2005, 326(4): 794-798.
[28]韩颖,秦炯,常杏芝,杨志仙,杜军保,汤秀英.气体信号分子硫化氢在热性惊厥脑损伤形成机制中的作用.实用医学杂志, 2006, 22(3): 248-251.
[29] Han Y, Qin J, Chang X, Yang Z, Bu D, Du J. Modulatingeffect of hydrogen sulfide onγ-aminobutyric acidβ- receptorin recurrent febrile seizures in rats. Neurosci Res, 2005, 53: 216–219.
[30] PT Wong, K Qu, GN Chimon, AB Seah, HM Chang, MC Wong, YK Ng, H Rumpel, B Halliwell, CP Chen. High plasma cyst(e)ine level may indicate poor clinical outcome in patients with acute stroke: possible involvement of hydrogen sulfide. J Neuropathol Exp Neurol, 2006, 65: 109-115.
[31] Kun Qu, Christopher P.L.H. Chen, Barry Halliwell, Philip K. Moore, Peter T.-H. Wong. Hydrogen sulfide is a mediator of cerebral ischemic damage. Stroke, 2006, 37: 889-893.
[32]邵建林,朱俊超,王俊科,马虹.胱硫醚-β-合酶/硫化氢和血红素氧合酶-1/一氧化碳体系在大鼠脑缺血再灌注损伤中的作用.中华麻醉学杂志,2006, 26(5): 439-442.
[33]邵建林,王俊科,马虹.外源性硫化氢对脑缺血再灌注损伤大鼠海马气体信号分子的影响.中华麻醉学杂志,2006, 2007, 27(5): 451-454.
[34] Weimin Zhao, Jing Zhang, Yanjie Lu, Rui Wang. The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener. European Molecular Biology Organization, 2001, 20 (21): 6008-6016.
[35] Ali MJ, Ping CY, Mok YP, Ling L, Whiteman M, Bhatia M. Regulation of vascular nitric oxide in vitro and in vivo; a new role for endogenous hydrogen sulphide? Br J Pharmacol, 2006, 149: 625–634.
[36] Zhao WM, Wang R. H2S - induced vasorelaxation and underlying cellular and molecular mechanisms. Am J Physiol Heart Circ Physiol, 2002, 283 (2): 474 - 480.
[37]金红芳,田悦,闫辉,唐朝枢,杜军保.硫化氢对正常及自发性高血压大鼠主动脉平滑肌细胞PCNA和P-ERK蛋白表达的影响.中国药理学通报, 2008, 24(2): 160-165.
[38]杜军保,陈晓波,耿彬.硫化氢作为心血管气体信号分子的研究.北京大学学报(医学版), 2002, 34 (2):187.
[39] Ting-Ting Pan, Kay Li Neo, Li-Fang Hu, Qian Chen Yong, Jin-Song Bian. H2S preconditioning-induced PKC activation regulates intracellular calcium handling in rat cardiomyocytes. Am J Physiol Cell Physiol, 2008, 294: C169–177.
[40] Bin Geng, Lin Chang, Chunshui Pan, Yongfen Qi, Jing Zhao,Yongzheng Pang, Junbao Du, Chaoshu Tang. Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol. Biochemical and Biophysical Research Communications, 2004, 318: 756–763.
[41] Lin Chang, Bin Geng, Fang Yu, Jing Zhao, Hongfeng Jiang, Junbao Du, Chaoshu Tang. Hydrogen sulfide inhibits myocardial injury induced by homocysteine in rats. Amino Acids, 2008, 34: 573–585.
[42]尹洪金,傅增泮,赵燕平,惠龙华.原发性高血压初诊患者测定血浆硫化氢的意义.临床军医杂志,2005,33(4): 393-395.
[43] Yan H, Du JB, Tang CS. The possible role of hydrogen sulfide on the pathogenesis of spontaneous hypertension in rats. Biochem Biophys Res Commun, 2004, 313 (1): 22 - 27.
[44]江海龙,吴宏超,李志梁,.耿彬,唐朝枢.冠心病病人血浆中新型气体信号分子硫化氢的变化.第一军医大学学报, 2005, 25 (8): 951– 954.
[45] J Du, Y Hui, Y Cheung, G Bin, H Jiang, X Chen, C Tang.The possible roleof hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cells. Heart Vessels, 2004, 19 (2): 75-80.
[46] Guangdong Yang, Xianfeng Sun, Rui Wang.Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen- activated protein kinases and caspase-3 . FASEB J , 2004, 18 (14): 1782-1784.
[47] Zagli G, Patacchini R, Trevisani M, Abbate R, Cinotti S, Gensini GF, Masotti G. Hydrogen sulfide inhibitshuman platelet aggregation. Eur J Pharm acol, 2007, 559 (1): 65 - 68.
[48] Pan TT, Feng ZN, Lee SW, Moore PK, Bian JS. Endogenous hydrogen sulfide contributes to the cardioprotection by metabolic inhibition preconditioning in the rat ventricular myocytes. J Mol Cell Cardiol, 2006, 40:119–130.
[49]李亮,张近宝,白崇峰.不同浓度硫化氢托马斯液心脏保存效果的实验研究.中国体外循环杂志, 2006, 4(4): 220-223
[50]白崇峰,崔勤,李亮,李彤.硫化氢对大鼠离体心脏低温保存效果的实验研究。中国体外循环杂志, 2007, 5(2): 114-117.
[51]常芳,李凌,常庆.硫化氢对大鼠心肌缺血再灌注损伤的保护作用。中原医刊, 2005, 32(9): 2-3.
[52] Jin-Song Bian, Qian Chen Yong, Ting-Ting Pan, Zhan-Ning Feng, Muhammed Yusuf Ali, Shufeng Zhou, Philip Keith Moore. Role of hydrogen sulfide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes. JPET, 2006, 316: 670–678.
[53] David Johansen, Kirsti Ytrehus, Gary F. Baxter. Exogenous hydrogen sulfide (H2S) protects against regional myocardial ischemia-reperfusion injury: Evidence for a role of KATP channels. Basic Res Cardiol, 2006, 101: 53– 60.
[54] Yeshi Hu,Xin Chen, Ting-Ting Pan, Kay Li Neo, Shiau Wei Lee, Ester Sandar Win Khin, Philip K. Moore, Jin-Song Bian. Cardioprotection induced by hydrogen sulfide preconditioning involves activation of ERK and PI3K/Akt pathways. Pflugers Arch - Eur J Physiol, 2008, 455: 607–616.
[55] Li-Fang Hu, Ting-Ting Pan, Kay Li Neo, Qian Chen Yong, Jin-Song Bian. Cyclooxygenase-2 mediates the delayed cardioprotection induced by hydrogen sulfide preconditioning in isolated rat cardiomyocytes. Pflugers Arch - Eur J Physiol, 2008, 455: 971–978.
[56]孙忠东,高尚志,毛志福,王志维,吴智勇.线粒体三磷酸腺苷敏感性钾通道在未成熟心肌缺血预处理中的作用.中国胸心血管外科临床杂志, 2009, 16(3): 210-213.
[57] John W. Elrod, John W. Calvert, Joanna Morrison, Jeannette E. Doeller, David W. Kraus, Ling Tao, Xiangying Jiao, Rosario Scalia, Levente Kiss, Csaba Szabo, Hideo Kimura, Chi-Wing Chow, and David J. Lefer. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. PNAS, 2007, 104(39): 15560–15565.
[58]李凌,常芳.硫化氢对大鼠心肌缺血再灌注损伤后心肌细胞凋亡的影响.河南医学研究, 2005, 14(2): 107-109.
[59]黄晓伟,姚玲玲,姚泰,朱依纯.外源性H2S在大鼠心肌缺血再灌注损伤中的作用.复旦学报(医学版), 2008, 5(2): 216-219.
[60] Neel R. Sodha, Richard T. Clements, Jun Feng, Yuhong Liu, Cesario Bianchi, Eszter M. Horvath, Csaba Szabo, Frank W. Sellke. The effects of therapeutic sulfide on myocardial apoptosis in response to ischemia—reperfusion injury. European Journal of Cardio-thoracic Surgery, 2008, 33: 906-913.
[61]杜军保,李万镇,赵斌.一氧化氮对慢性缺氧大鼠肺动脉内皮素基因表达的影响.中华医学杂志, 1997, 77(4): 263-265.
[62]杜军保,赵斌,黎文.一氧化氮合酶mRNA在缺氧性肺动脉高压大鼠肺动脉的表达和分布.中华儿科杂志, 1998, 36(1): 19-21.
[63]顾勇,王治平,张希,孙培吾,刘秀琴.一氧化氮吸入对肺动脉高压大鼠血压和血浆中血管活性物质水平的影响.中国动脉硬化志, 2003, 11(3): 219-222.
[64] Shi Yun, Du Junbao, Gong Limin. The regulating effect of heme oxygenase/carbon monoxide on hypoxic pulmonary vascular structural remodeling. Biochem. Biophys. Res. Commun, 2003, 306: 523–529.
[65] Zhang Chunyu, Du Junbao, Bu Dingfang, Yan Hui, Tang Xiuying, Tang Chaoshu. The regulatory effect of hydrogen sulfide on hypoxic pulmonary hypertension in rats. Biochemical and Biophysical Research Communications, 2003, 302: 810–816.
[66]陈晓波,杜军保,张春雨.硫化氢对低氧性肺动脉高压大鼠肺动脉增殖细胞核抗原及Bcl-2的调节作用.实用儿科临床杂志, 2004, 19 (3): 185– 187.
[67]李晓惠,杜军保,唐朝枢.内源性硫化氢对高肺血流大鼠肺血管重构及血管活性物质的影响.中国药理学通报, 2007, 23(3): 327-331.
[68]李晓惠,杜军保,唐朝枢.硫化氢供体对大鼠高肺血流性肺动脉高压中内皮素-1及结缔组织生长因子表达的影响.中国病理生理杂志, 2008, 24(3): 446-450.
[69]王勇,但艳苹,王大斌.肺动脉高压患儿血浆硫化氢的变化及其与预后的关系.实用医学杂志, 2009, 25(10): 1593-1595.
[70] Tianshui Li, BIin Zhao, Cong Wang, Haiying Wang, Zhiwei Liu, Wang Li, Hongfang Jin, Chaoshu Tang, Junbao Du. Regulatory Effects of hydrogen sulfide on IL-6, IL-8 and IL-10 levels in the plasma and pulmonary tissue of rats with acute lung injury. Exp Biol Med, 2008, 233:1081–1087.
[71]王平,张建新,李兰芳,张勤增,金普乐,丁翠敏.内毒素性急性肺损伤大鼠内源性H2S/CSE体系的变化.中国病理生理杂志, 2008, 24(3): 434-438.
[72]殷亚俊,刘志勇.硫化氢对大鼠肺缺血再灌注氧化损伤的影响.现代医学, 2009, 37(3): 184-188.
[73]黄新莉,周晓红,周君琳,丁春华,羡晓辉.中性粒细胞在外源性硫化氢抗内毒素致急性肺损伤中的作用.生理学报, 2009, 61 (4): 356-360.
[74]鲍文华,赵丽丽.硫化氢在大鼠肺纤维化中的表达.黑龙江医药科学, 2009, 32(1): 45-46.
[75]刘新民,耿彬,潘春水,齐永芬,吴胜英,唐朝枢.新型气体信号分子硫化氢在大鼠肺纤维化发病中的作用.北京大学学报(医学版), 2006, 38(2): 140-146.
[76]张永健,邓勇,樊海宁,王芝,卢根林,格日力.肝硬化患者血清硫化氢、一氧化氮含量的变化.基础医学与临床, 28(5): 499-500.
[77]乌剑利,杨镇,曾凡军,张爱龙,肖亮,王超,李岽健.门静脉高压症患者血浆内源性硫化氢含量的变化和意义.微循环学杂志, 2008, 18(3): 53-55.
[78] Fiorucci S, Antonelli E, Mencarelli A. The third gas: H2S regulates perfusion pressure in both the isolated and perfused normal rat liver and in cirrhosis. Hepatology, 2005, 42(3): 539- 548.
[79] Saurabh Jha, John W. Calvert, Mark R. Duranski, Arun Ramachandran, David J. Lefer. Hydrogen Sulfide Attenuates Hepatic Ischemia-Reperfusion Injury: Role of Antioxidant and Anti-Apoptotic Signaling. Am J Physiol Heart Circ Physiol, 2008, 295: H801–H806.
[80] Fiorucci S, Antonelli E, Distrutti E, Rizzo G, Mencarelli A, Orlandi S, Zanardo R: Inhibition of hydrogen sulfide generation contributes to gastric injury caused by non-steroidal anti-inflammatory drugs. Gastroenterology,2005, 129: 1210–1224.
[81] S. Kubo, M. Kajiwara, A. Kawabata. Dual modulation of the tension of isolated gastric artery and gastric mucosal circulation by hydrogen sulfide in rats. Inflammopharmacology, 2007, 15: 288–292.
[82] Distrutti E, Sediari L, Mencarelli A, Renga B, Orlandi S, Antonelli E, Roviezzo F. Evidence that hydrogen sulfide exerts antinociceptive effects in the gastrointestinal tract by activating K+-channels. J Pharmacol Exp Ther, 2006, 316: 325–335.
[83] Marika Collin, Farhana B.M. Anuar, Oliver Murch, Madhav Bhatia, Philip K. Moore,Christoph Thiemermann. Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemia. British Journal of Pharmacology, 2005, 146: 498–505.
[84] Huili Zhang, Shabbir M. Moochhala, Madhav Bhatia. Endogenous hydrogen sulfide regulates inflammatory response by activating the ERK pathway in polymicrobial sepsis. The Journal of Immunology, 2008: 4320-4331.
[85] Wallace JL. Hydrogen sulfide-releasing anti-inflammatory drugs. Trends in Pharmacological Sciences 2007, 28 (10): 501-505.
[86] Ling Li, Manuel Salto-Tellez, Choon-Hong Tan, Matthew Whiteman, Philip K. Moore. GYY4137, a novel hydrogen sulfide-releasing molecule, protects against endotoxic shock in the rat. Free Radical Biology & Medicine,2009(in press).
[87] Blackstone E, Morrison M, Roth MB. H2S induces a suspended animation-like state in mice. Science, 2005, 308: 518.
[88] Volpato GP, Searles RJ, Scherres-Crosbie M. Cardiovascular changes after exposure hydrogen sulfide in a murine model. Circulation. 2006,114: 465.
[89] Y Bhambhani, R Burnham, G Snydmiller, I MacLean. Effects of 10-ppm hydrogen sulfide inhalation in exercising men and women. JOEM, 1997, 39(2): 122 - 129.
[90] ML Morrison, JE Blackwood, SL Lockett, A Iwata, RK Winn, MB Roth. Surviving blood loss using hydrogen sulfide.Trauma, 2008; 65(1): 183-188.
[91] Bin Geng, Yuying Cui, Jing Zhao, Fang Yu, Yi Zhu, Geyang Xu, Zhiwen Zhang, Chaoshu Tang, Junbao Du.Hydrogen sulfide downregulates the aortic L-arginine/nitric oxide pathway in rats. Am J Physiol Regul Integr Comp Physiol, 2007, 293: R1608–R1618.
[92] Wang R. Two’s company, three’s a crowd: can H2S be the third endogenous gaseous transmitter? FASEB J, 2002, 16: 1792-1798.
[93] Krug EG, Sharma GK, Lozano R: The global burden of injuries. Am J Public Health, 2000, 90: 523-526.
[94]管利东,王字玲,赵莲,王波,王广义,魏广智,周虹.丙酮酸钠对失血性休克大鼠缺血/再灌注损伤的保护作用.中国应用生理学杂志, 2007, 23 (3):264-268.
[95] BX Pan, GL Zhao, XL Huang, KS Zhao. Mobilization of intracellular calcium by peroxynitrite in arteriolar smooth muscle cells from rats. Redox Rep, 2004, 9(1): 49-55.
[96]樊凤艳,王广义,周虹,王字玲.肌肽抗全身性缺血/再灌注损伤作用的研究.中国急救医学, 2007, 27(2): 143-145.
[97] Daniela Salvemini, Zhi-Qiang Wang, Jay L. Zweier, Alexandre Samouilov, Heather Macarthur, Thomas P. Misko, Mark G. Currie, Salvatore Cuzzocrea, James A. Sikorski, Dennis P. RileyA. Nonpeptidyl mimic of superoxide dismutase with therapeutic activity in rats. Science, 1999, 286(5438): 304– 306.
[98]曾翔俊,王红霞,王艳霞,陈玉涵,芦玲巧,唐朝枢,郝刚.硫化氢拮抗乳鼠心肌缺氧/复氧损伤机制初探.中国病理生理杂志,2009, 25 (5): 839– 843.
[99] Dierk E. Remmers, Ping Wang, William G. Cioffi, Kirby I. Bland, Irshad H. Chaudry. Testosterone receptor blockade after trauma-hemorrhage improves cardiac and hepatic functions in males Am J Physiol Heart Circ Physiol, 1997, 273: 2919-2925.
[100] Wen-Hong Kan, Chi-Hsun Hsieh, Martin G. Schwacha, Mashkoor A. Choudhry, Raghavan Raju, Kirby I. Bland, Irshad H. Chaudry. Flutamide protects against trauma-hemorrhage-induced liver injury via attenuation of the inflammatory response, oxidative stress, and apopotosis J Appl Physiol, 2008, 105: 595–602.
[101]江其生,胡德耀,肖南,刘韧,王庆松,闵家新,田昆仑,刘良明.失血性休克大鼠血管平滑肌细胞钙超载的三磷酸腺苷酶机制.中华创伤杂志, 2003, 19(6): 337-340.
[102] Crompton M. The mitochondrial permeability transition pore and its role in cell death. Biochem J, 1999, 341(2): 233-249.
[103] Fink MP. Cytopathic hypoxia - mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis. Crit Care Clin, 2001, 17: 219。
[104] Jérome Larche, Steve Lancel, Sidi Mohamed Hassoun, Raphael Favory, Brigitte Decoster, Philippe Marchetti, Claude Chopin, Remi Neviere. Inhibition of Mitochondrial Permeability Transition Prevents Sepsis-Induced Myocardial Dysfunction and Mortality. J. Am. Coll. Cardiol, 2006, 48: 377-385.
[105] J Barroso-Aranda, GW Schmid-Schonbein, BW Zweifach,RL Engler. Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock. Circulation Research, 1988, 63: 437-447.
[106] JL Zhao, YJ Yang, CJ Cui, SJ You, YJ Wu, RL Gao. Different effects of adenosine and calcium channel blockade on myocardial no-reflow after acute myocardial infarction and reperfusion. Cardiovasc Drugs Ther, 2006,20(3): 167-175.
[107] JL Zhao, YJ Yang, SJ You, ZC Jing, YJ Wu, WX Yang, JL Chen, RL Gao, ZJ Chen. Effect of adenosine on endothelin-1 in the infarcted reflow and no-reflow myocardium of mini-swine. Zhongguo Yi Xue Ke Xue Yuan Xue Bao, 2006, 28(2): 225-229.
[108] JL Zhao, YJ Yang, YJ Wu, ZC Jing, SJ You, WX Yang, L Meng, Y Tian, JL Chen, RL Gao, ZJ Chen. Effects of anti-platelet drugs on myocardial no-reflow after acute myocardial infarction and reperfusion: experiment with mini-swine model. Zhonghua Yi Xue Za Zhi, 2005, 85(31): 2187-2191.
[109] H Macarthur, DM Couri, GH Wilken, TC Westfall, AJ Lechner, GM Matuschak, Z Chen, D Salvemini. Modulation of serum cytokine level by a novel superoxide dismutase mimetic, M40401, in an Escherichia coli model of septic shock: correlation with preserved circulating catecholamines. Crit Care Med, 2003, 31: 237 - 245.
[110] K Takakura, T Taniguchi, I Muramatsu, K Takeuchi, S Fukuda. Modification of alpha1 -adrenoceptors by peroxynitrite as a possible mechanism of systemic hypotension in sepsis. Crit Care Med, 2002, 30(4): 894-899.
[111] Csaba Szabó, Basilia Zingarelli, Andrew L. Salzman. Role of Poly-ADP Ribosyltransferase Activation in the Vascular Contractile and Energetic Failure Elicited by Exogenous and Endogenous Nitric Oxide and Peroxynitrite. Circ. Res, 1996, 78: 1051 - 1063.
[112] Ya-Ching Hsieh, Shaolong Yang, Mashkoor A. Choudhry, Huang-Ping Yu, Kirby I. Bland, Martin G. Schwacha, Irshad H. Chaudry. Flutamide restores cardiac function after trauma-hemorrhage via an estrogen-dependent pathway through upregulation of PGC-1. Am J Physiol Heart Circ Physiol, 2006, 290: H416-423.
[113] Anne Craveiro Br?chner, Palle Toft. Pathophysiology of the systemicinflammatory response after major accidental trauma. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 2009, 17: 43.
[114] Zhao KS. Advances in the study on rheological behavior of leukocyte during severe shock. Chin Med J, 1996, 109: 110.
[115] Dieter Rixen,J ohn H Siegel. Bench-to-bedside review: Oxygen debt and its metabolic correlates as quantifiers of the severity of hemorrhagic and posttraumatic shock. Critical Care, 2005 9: 441-453.
[116]甯交琳,赖西南,葛衡江,王韶亮,莫立稳,王丽丽,朱剑武.控制性低温对创伤失血性休克后早期炎症反应及器官功能的影响.创伤外科杂志, 2007, 27(2): 143-145.
[117]熊申宁,许建宁.雌激素对创伤失血性休克大鼠肝脏功能的影响.江西医学院学报, 2005, 45(6): 51-53.
[118]冯浩淼,黄宗海,黄绪亮,孙英刚,林洪武. L-精氨酸对创伤性休克大鼠的保护作用研究.中国急救医学, 2004, 24(1): 1-3.
[119] T Murata, H Nakazawa, I Mori, Y Ohta, H Yamabayashi. Reperfusion after a two hour period of pulmonary artery occlusion cause pulmonary necrosis. Am Rev Respir Dis, 1992, 146 (4): 1048 - 1053.
[2] Beauchamp RO, Bus JS, Popp JA, Boreiko CJ, Goldberg L. A critical review of the literature on hydrogen sulfide toxicity. CRC Crit Rev Toxicol, 1984, 13: 25-97.
[3] Reiffenstein RJ, Hulbert WC, Roth SH. Toxicology of hydrogen sulfide. Annu Rev Pharmacol Toxicol, 1992, 32: 109-134.
[4] Partlo LA, Sainsbury RS, Roth SH. Effects of repeated hydrogen sulphide (H2S) exposure on learning and memory in the adult rat. Neurotoxicology, 2001, 22(2): 177- 189.
[5] Moore PK, Bhatia M, Moochhala S. Hydrogen sulfide: from the smell of the past to the mediator of the future? Trends Pharmacol Sci, 2003, 24(12): 609- 611.
[6] Abe K, Kimura H. The possible role of hydrogen sulfide as an endogenous neuromodulator. J Neurosci, 1996, 16(3): 1066-1071.
[7] Richardson CJ, Magee EA, Cummings JH. A new method for the determination of sulphide in gastrointestinal contents and whole blood by microdistillation and ion chromatography. Clin Chim Acta, 2000, 293 (1-2): 115– 125.
[8] Stipanuk MH, Beck PW. Characterization of the enzymatic capacity for cysteine desulphhydration in liver and kidney of the rat. Biochem J, 1982, 206 (2): 267–277.
[9] Doeller JE, Isbell TS, Benavides G, Koenitzer J, Patel H, Patel RP, Lancaster JR Jr, Darley-Usmar VM, Kraus DW. Polarographic measurement ofhydrogen sulfide production and consumption by mammalian tissues. Anal Biochem, 2005, 341: 40–51.
[10] Eto K, Kimura H. The production of hydrogen sulfide is regulated by testosterone and S-adenosyl-L-methionine in mouse brain. J Neurochem, 2002, 83 (1): 80 - 86.
[11] Banerjee R, Zou CG. Redox regulation and reaction mechanism of human cystathionine-beta-synthase: a PLP -dependent hemesensor protein. Arch Biochem Biophys, 2005, 433:144-156.
[12] Puranik M, Weeks CL, Lahaye D, Kabil O, Taoka S, Nielsen SB, Groves JT, Banerjee R, Spiro TG.. Dynamics of carbon monoxide binding to cystathionine-β-synthase. J Biol Chem, 2006, 281: 13433–13438.
[13] Taoka S, Banerjee R. Characterization of NO binding to human cystathionine-β-synthase: possible implications of the effects of CO and NO binding to the human enzyme.J Inorg Biochem, 2001, 87: 245–251.
[14] Taoka S, Green EL, Loehr TM, Banerjee R. Mercuric chloride-induced spin or ligation state changes in ferric or ferrous human cystathionine beta-synthase inhibit enzyme activity. J Inorg Biochem, 2001, 87 (4): 253 - 259.
[15] Jacobs RL, Stead LM, Brosnan ME. Hyperglucagonemia in rats results in decreased plasma homocysteine and increased flur through the trans-sulfuration pathway in liver. J Biol Chem, 2001, 276 (47): 43740 -43747.
[16] Dicker BA, Fonseca VA, Fink LM, Kern PA. The effect of glucose and insulin on the activity of methylene tetrahydrofolate reductase and cystathionine-beta-synthase: Studies in hepatocytes. Atherosclerosis, 2001,158 (2): 297 - 301.
[17] Fiorucci S, Distrutti, E, Cirino, G. Wallace, JL. The emerging roles ofhydrogen sulfide in the gastrointestinal tract and liver. Gastroenterology, 2006, 131: 259–271.
[18] Zhao W, Ndisang JF, Wang R. Modulation of endogenous production of H2S in rat tissues. Can J Physiol Pharmacol, 2003, 81: 848–853.
[19] Furne J, Springfield J, Koenig T, DeMaster E, Levitt MD. Oxidation of hydrogen sulfide and methanethiol to thiosulfate by rat tissues: a specialized function ofthe colonic mucosa. Biochem Pharmacol, 2001, 62(2): 255-259.
[20] Kimura H. Hydrogen sulfide induces cyclic AMP and modulates the NMDA receptor. Biochem Biophys Res Commun, 2000, 267: 129–133.
[21] Nagai Y, Tsugane M, Oka J, Kimura H. Hydrogen sulfide induces calcium waves in astrocytes. FASEB J, 2004, 18: 557–559.
[22] Lee SW, Hu YS, Hu LF, Lu Q, Dawe GS, Moore PK, Wong PT. Hydrogen sulphide regulates calcium homeostasis in microglial cells. Glia, 2006, 54: 116–124.
[23] Yuka Kimura, Hideo Kimura. Hydrogen sulfide protects neurons from oxidative stress. Faseb J, 2004, 18: 1165–1167.
[24] Whiteman M, Cheung NS, Zhu YZ, Chu SH, Siau J L, Wong BS, Armstrong JS, Moore PK. Hydrogen sulphide: a novel inhibitor of hypochlorous acid-mediated oxidative damage in the brain? Biochem. Biophys. Res Commun, 2005, 326: 794–798.
[25] Ming Lu, Li-Fang Hu, Gang Hu, Jin-Song Bian. Hydrogen sulfide protects astrocytes against H2O2-induced neural injury via enhancing glutamate uptake. Free Radical Biology & Medicine, 2008, 45: 1705–1713.
[26] Eto K, Asada T, Arima K, Makifuchi T, Kimura H. Brain hydrogen sulfide is severely decreased in Alzheimer’s disease. Biochem Biophys Res Commun, 2002, 293: 1485–1488.
[27] M Whiteman, NS Cheung, YZ Zhu, SH Chu, JL Siau, BS Wong, JSArmstrong, PK Moore. Hydrogen sulphide: a novel inhibitor of hypochlorous acid-mediated oxidative damage in the brain? Biochem Biophys Res Commun, 2005, 326(4): 794-798.
[28]韩颖,秦炯,常杏芝,杨志仙,杜军保,汤秀英.气体信号分子硫化氢在热性惊厥脑损伤形成机制中的作用.实用医学杂志, 2006, 22(3): 248-251.
[29] Han Y, Qin J, Chang X, Yang Z, Bu D, Du J. Modulatingeffect of hydrogen sulfide onγ-aminobutyric acidβ- receptorin recurrent febrile seizures in rats. Neurosci Res, 2005, 53: 216–219.
[30] PT Wong, K Qu, GN Chimon, AB Seah, HM Chang, MC Wong, YK Ng, H Rumpel, B Halliwell, CP Chen. High plasma cyst(e)ine level may indicate poor clinical outcome in patients with acute stroke: possible involvement of hydrogen sulfide. J Neuropathol Exp Neurol, 2006, 65: 109-115.
[31] Kun Qu, Christopher P.L.H. Chen, Barry Halliwell, Philip K. Moore, Peter T.-H. Wong. Hydrogen sulfide is a mediator of cerebral ischemic damage. Stroke, 2006, 37: 889-893.
[32]邵建林,朱俊超,王俊科,马虹.胱硫醚-β-合酶/硫化氢和血红素氧合酶-1/一氧化碳体系在大鼠脑缺血再灌注损伤中的作用.中华麻醉学杂志,2006, 26(5): 439-442.
[33]邵建林,王俊科,马虹.外源性硫化氢对脑缺血再灌注损伤大鼠海马气体信号分子的影响.中华麻醉学杂志,2006, 2007, 27(5): 451-454.
[34] Weimin Zhao, Jing Zhang, Yanjie Lu, Rui Wang. The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener. European Molecular Biology Organization, 2001, 20 (21): 6008-6016.
[35] Ali MJ, Ping CY, Mok YP, Ling L, Whiteman M, Bhatia M. Regulation of vascular nitric oxide in vitro and in vivo; a new role for endogenous hydrogen sulphide? Br J Pharmacol, 2006, 149: 625–634.
[36] Zhao WM, Wang R. H2S - induced vasorelaxation and underlying cellular and molecular mechanisms. Am J Physiol Heart Circ Physiol, 2002, 283 (2): 474 - 480.
[37]金红芳,田悦,闫辉,唐朝枢,杜军保.硫化氢对正常及自发性高血压大鼠主动脉平滑肌细胞PCNA和P-ERK蛋白表达的影响.中国药理学通报, 2008, 24(2): 160-165.
[38]杜军保,陈晓波,耿彬.硫化氢作为心血管气体信号分子的研究.北京大学学报(医学版), 2002, 34 (2):187.
[39] Ting-Ting Pan, Kay Li Neo, Li-Fang Hu, Qian Chen Yong, Jin-Song Bian. H2S preconditioning-induced PKC activation regulates intracellular calcium handling in rat cardiomyocytes. Am J Physiol Cell Physiol, 2008, 294: C169–177.
[40] Bin Geng, Lin Chang, Chunshui Pan, Yongfen Qi, Jing Zhao,Yongzheng Pang, Junbao Du, Chaoshu Tang. Endogenous hydrogen sulfide regulation of myocardial injury induced by isoproterenol. Biochemical and Biophysical Research Communications, 2004, 318: 756–763.
[41] Lin Chang, Bin Geng, Fang Yu, Jing Zhao, Hongfeng Jiang, Junbao Du, Chaoshu Tang. Hydrogen sulfide inhibits myocardial injury induced by homocysteine in rats. Amino Acids, 2008, 34: 573–585.
[42]尹洪金,傅增泮,赵燕平,惠龙华.原发性高血压初诊患者测定血浆硫化氢的意义.临床军医杂志,2005,33(4): 393-395.
[43] Yan H, Du JB, Tang CS. The possible role of hydrogen sulfide on the pathogenesis of spontaneous hypertension in rats. Biochem Biophys Res Commun, 2004, 313 (1): 22 - 27.
[44]江海龙,吴宏超,李志梁,.耿彬,唐朝枢.冠心病病人血浆中新型气体信号分子硫化氢的变化.第一军医大学学报, 2005, 25 (8): 951– 954.
[45] J Du, Y Hui, Y Cheung, G Bin, H Jiang, X Chen, C Tang.The possible roleof hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cells. Heart Vessels, 2004, 19 (2): 75-80.
[46] Guangdong Yang, Xianfeng Sun, Rui Wang.Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen- activated protein kinases and caspase-3 . FASEB J , 2004, 18 (14): 1782-1784.
[47] Zagli G, Patacchini R, Trevisani M, Abbate R, Cinotti S, Gensini GF, Masotti G. Hydrogen sulfide inhibitshuman platelet aggregation. Eur J Pharm acol, 2007, 559 (1): 65 - 68.
[48] Pan TT, Feng ZN, Lee SW, Moore PK, Bian JS. Endogenous hydrogen sulfide contributes to the cardioprotection by metabolic inhibition preconditioning in the rat ventricular myocytes. J Mol Cell Cardiol, 2006, 40:119–130.
[49]李亮,张近宝,白崇峰.不同浓度硫化氢托马斯液心脏保存效果的实验研究.中国体外循环杂志, 2006, 4(4): 220-223
[50]白崇峰,崔勤,李亮,李彤.硫化氢对大鼠离体心脏低温保存效果的实验研究。中国体外循环杂志, 2007, 5(2): 114-117.
[51]常芳,李凌,常庆.硫化氢对大鼠心肌缺血再灌注损伤的保护作用。中原医刊, 2005, 32(9): 2-3.
[52] Jin-Song Bian, Qian Chen Yong, Ting-Ting Pan, Zhan-Ning Feng, Muhammed Yusuf Ali, Shufeng Zhou, Philip Keith Moore. Role of hydrogen sulfide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes. JPET, 2006, 316: 670–678.
[53] David Johansen, Kirsti Ytrehus, Gary F. Baxter. Exogenous hydrogen sulfide (H2S) protects against regional myocardial ischemia-reperfusion injury: Evidence for a role of KATP channels. Basic Res Cardiol, 2006, 101: 53– 60.
[54] Yeshi Hu,Xin Chen, Ting-Ting Pan, Kay Li Neo, Shiau Wei Lee, Ester Sandar Win Khin, Philip K. Moore, Jin-Song Bian. Cardioprotection induced by hydrogen sulfide preconditioning involves activation of ERK and PI3K/Akt pathways. Pflugers Arch - Eur J Physiol, 2008, 455: 607–616.
[55] Li-Fang Hu, Ting-Ting Pan, Kay Li Neo, Qian Chen Yong, Jin-Song Bian. Cyclooxygenase-2 mediates the delayed cardioprotection induced by hydrogen sulfide preconditioning in isolated rat cardiomyocytes. Pflugers Arch - Eur J Physiol, 2008, 455: 971–978.
[56]孙忠东,高尚志,毛志福,王志维,吴智勇.线粒体三磷酸腺苷敏感性钾通道在未成熟心肌缺血预处理中的作用.中国胸心血管外科临床杂志, 2009, 16(3): 210-213.
[57] John W. Elrod, John W. Calvert, Joanna Morrison, Jeannette E. Doeller, David W. Kraus, Ling Tao, Xiangying Jiao, Rosario Scalia, Levente Kiss, Csaba Szabo, Hideo Kimura, Chi-Wing Chow, and David J. Lefer. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. PNAS, 2007, 104(39): 15560–15565.
[58]李凌,常芳.硫化氢对大鼠心肌缺血再灌注损伤后心肌细胞凋亡的影响.河南医学研究, 2005, 14(2): 107-109.
[59]黄晓伟,姚玲玲,姚泰,朱依纯.外源性H2S在大鼠心肌缺血再灌注损伤中的作用.复旦学报(医学版), 2008, 5(2): 216-219.
[60] Neel R. Sodha, Richard T. Clements, Jun Feng, Yuhong Liu, Cesario Bianchi, Eszter M. Horvath, Csaba Szabo, Frank W. Sellke. The effects of therapeutic sulfide on myocardial apoptosis in response to ischemia—reperfusion injury. European Journal of Cardio-thoracic Surgery, 2008, 33: 906-913.
[61]杜军保,李万镇,赵斌.一氧化氮对慢性缺氧大鼠肺动脉内皮素基因表达的影响.中华医学杂志, 1997, 77(4): 263-265.
[62]杜军保,赵斌,黎文.一氧化氮合酶mRNA在缺氧性肺动脉高压大鼠肺动脉的表达和分布.中华儿科杂志, 1998, 36(1): 19-21.
[63]顾勇,王治平,张希,孙培吾,刘秀琴.一氧化氮吸入对肺动脉高压大鼠血压和血浆中血管活性物质水平的影响.中国动脉硬化志, 2003, 11(3): 219-222.
[64] Shi Yun, Du Junbao, Gong Limin. The regulating effect of heme oxygenase/carbon monoxide on hypoxic pulmonary vascular structural remodeling. Biochem. Biophys. Res. Commun, 2003, 306: 523–529.
[65] Zhang Chunyu, Du Junbao, Bu Dingfang, Yan Hui, Tang Xiuying, Tang Chaoshu. The regulatory effect of hydrogen sulfide on hypoxic pulmonary hypertension in rats. Biochemical and Biophysical Research Communications, 2003, 302: 810–816.
[66]陈晓波,杜军保,张春雨.硫化氢对低氧性肺动脉高压大鼠肺动脉增殖细胞核抗原及Bcl-2的调节作用.实用儿科临床杂志, 2004, 19 (3): 185– 187.
[67]李晓惠,杜军保,唐朝枢.内源性硫化氢对高肺血流大鼠肺血管重构及血管活性物质的影响.中国药理学通报, 2007, 23(3): 327-331.
[68]李晓惠,杜军保,唐朝枢.硫化氢供体对大鼠高肺血流性肺动脉高压中内皮素-1及结缔组织生长因子表达的影响.中国病理生理杂志, 2008, 24(3): 446-450.
[69]王勇,但艳苹,王大斌.肺动脉高压患儿血浆硫化氢的变化及其与预后的关系.实用医学杂志, 2009, 25(10): 1593-1595.
[70] Tianshui Li, BIin Zhao, Cong Wang, Haiying Wang, Zhiwei Liu, Wang Li, Hongfang Jin, Chaoshu Tang, Junbao Du. Regulatory Effects of hydrogen sulfide on IL-6, IL-8 and IL-10 levels in the plasma and pulmonary tissue of rats with acute lung injury. Exp Biol Med, 2008, 233:1081–1087.
[71]王平,张建新,李兰芳,张勤增,金普乐,丁翠敏.内毒素性急性肺损伤大鼠内源性H2S/CSE体系的变化.中国病理生理杂志, 2008, 24(3): 434-438.
[72]殷亚俊,刘志勇.硫化氢对大鼠肺缺血再灌注氧化损伤的影响.现代医学, 2009, 37(3): 184-188.
[73]黄新莉,周晓红,周君琳,丁春华,羡晓辉.中性粒细胞在外源性硫化氢抗内毒素致急性肺损伤中的作用.生理学报, 2009, 61 (4): 356-360.
[74]鲍文华,赵丽丽.硫化氢在大鼠肺纤维化中的表达.黑龙江医药科学, 2009, 32(1): 45-46.
[75]刘新民,耿彬,潘春水,齐永芬,吴胜英,唐朝枢.新型气体信号分子硫化氢在大鼠肺纤维化发病中的作用.北京大学学报(医学版), 2006, 38(2): 140-146.
[76]张永健,邓勇,樊海宁,王芝,卢根林,格日力.肝硬化患者血清硫化氢、一氧化氮含量的变化.基础医学与临床, 28(5): 499-500.
[77]乌剑利,杨镇,曾凡军,张爱龙,肖亮,王超,李岽健.门静脉高压症患者血浆内源性硫化氢含量的变化和意义.微循环学杂志, 2008, 18(3): 53-55.
[78] Fiorucci S, Antonelli E, Mencarelli A. The third gas: H2S regulates perfusion pressure in both the isolated and perfused normal rat liver and in cirrhosis. Hepatology, 2005, 42(3): 539- 548.
[79] Saurabh Jha, John W. Calvert, Mark R. Duranski, Arun Ramachandran, David J. Lefer. Hydrogen Sulfide Attenuates Hepatic Ischemia-Reperfusion Injury: Role of Antioxidant and Anti-Apoptotic Signaling. Am J Physiol Heart Circ Physiol, 2008, 295: H801–H806.
[80] Fiorucci S, Antonelli E, Distrutti E, Rizzo G, Mencarelli A, Orlandi S, Zanardo R: Inhibition of hydrogen sulfide generation contributes to gastric injury caused by non-steroidal anti-inflammatory drugs. Gastroenterology,2005, 129: 1210–1224.
[81] S. Kubo, M. Kajiwara, A. Kawabata. Dual modulation of the tension of isolated gastric artery and gastric mucosal circulation by hydrogen sulfide in rats. Inflammopharmacology, 2007, 15: 288–292.
[82] Distrutti E, Sediari L, Mencarelli A, Renga B, Orlandi S, Antonelli E, Roviezzo F. Evidence that hydrogen sulfide exerts antinociceptive effects in the gastrointestinal tract by activating K+-channels. J Pharmacol Exp Ther, 2006, 316: 325–335.
[83] Marika Collin, Farhana B.M. Anuar, Oliver Murch, Madhav Bhatia, Philip K. Moore,Christoph Thiemermann. Inhibition of endogenous hydrogen sulfide formation reduces the organ injury caused by endotoxemia. British Journal of Pharmacology, 2005, 146: 498–505.
[84] Huili Zhang, Shabbir M. Moochhala, Madhav Bhatia. Endogenous hydrogen sulfide regulates inflammatory response by activating the ERK pathway in polymicrobial sepsis. The Journal of Immunology, 2008: 4320-4331.
[85] Wallace JL. Hydrogen sulfide-releasing anti-inflammatory drugs. Trends in Pharmacological Sciences 2007, 28 (10): 501-505.
[86] Ling Li, Manuel Salto-Tellez, Choon-Hong Tan, Matthew Whiteman, Philip K. Moore. GYY4137, a novel hydrogen sulfide-releasing molecule, protects against endotoxic shock in the rat. Free Radical Biology & Medicine,2009(in press).
[87] Blackstone E, Morrison M, Roth MB. H2S induces a suspended animation-like state in mice. Science, 2005, 308: 518.
[88] Volpato GP, Searles RJ, Scherres-Crosbie M. Cardiovascular changes after exposure hydrogen sulfide in a murine model. Circulation. 2006,114: 465.
[89] Y Bhambhani, R Burnham, G Snydmiller, I MacLean. Effects of 10-ppm hydrogen sulfide inhalation in exercising men and women. JOEM, 1997, 39(2): 122 - 129.
[90] ML Morrison, JE Blackwood, SL Lockett, A Iwata, RK Winn, MB Roth. Surviving blood loss using hydrogen sulfide.Trauma, 2008; 65(1): 183-188.
[91] Bin Geng, Yuying Cui, Jing Zhao, Fang Yu, Yi Zhu, Geyang Xu, Zhiwen Zhang, Chaoshu Tang, Junbao Du.Hydrogen sulfide downregulates the aortic L-arginine/nitric oxide pathway in rats. Am J Physiol Regul Integr Comp Physiol, 2007, 293: R1608–R1618.
[92] Wang R. Two’s company, three’s a crowd: can H2S be the third endogenous gaseous transmitter? FASEB J, 2002, 16: 1792-1798.
[93] Krug EG, Sharma GK, Lozano R: The global burden of injuries. Am J Public Health, 2000, 90: 523-526.
[94]管利东,王字玲,赵莲,王波,王广义,魏广智,周虹.丙酮酸钠对失血性休克大鼠缺血/再灌注损伤的保护作用.中国应用生理学杂志, 2007, 23 (3):264-268.
[95] BX Pan, GL Zhao, XL Huang, KS Zhao. Mobilization of intracellular calcium by peroxynitrite in arteriolar smooth muscle cells from rats. Redox Rep, 2004, 9(1): 49-55.
[96]樊凤艳,王广义,周虹,王字玲.肌肽抗全身性缺血/再灌注损伤作用的研究.中国急救医学, 2007, 27(2): 143-145.
[97] Daniela Salvemini, Zhi-Qiang Wang, Jay L. Zweier, Alexandre Samouilov, Heather Macarthur, Thomas P. Misko, Mark G. Currie, Salvatore Cuzzocrea, James A. Sikorski, Dennis P. RileyA. Nonpeptidyl mimic of superoxide dismutase with therapeutic activity in rats. Science, 1999, 286(5438): 304– 306.
[98]曾翔俊,王红霞,王艳霞,陈玉涵,芦玲巧,唐朝枢,郝刚.硫化氢拮抗乳鼠心肌缺氧/复氧损伤机制初探.中国病理生理杂志,2009, 25 (5): 839– 843.
[99] Dierk E. Remmers, Ping Wang, William G. Cioffi, Kirby I. Bland, Irshad H. Chaudry. Testosterone receptor blockade after trauma-hemorrhage improves cardiac and hepatic functions in males Am J Physiol Heart Circ Physiol, 1997, 273: 2919-2925.
[100] Wen-Hong Kan, Chi-Hsun Hsieh, Martin G. Schwacha, Mashkoor A. Choudhry, Raghavan Raju, Kirby I. Bland, Irshad H. Chaudry. Flutamide protects against trauma-hemorrhage-induced liver injury via attenuation of the inflammatory response, oxidative stress, and apopotosis J Appl Physiol, 2008, 105: 595–602.
[101]江其生,胡德耀,肖南,刘韧,王庆松,闵家新,田昆仑,刘良明.失血性休克大鼠血管平滑肌细胞钙超载的三磷酸腺苷酶机制.中华创伤杂志, 2003, 19(6): 337-340.
[102] Crompton M. The mitochondrial permeability transition pore and its role in cell death. Biochem J, 1999, 341(2): 233-249.
[103] Fink MP. Cytopathic hypoxia - mitochondrial dysfunction as mechanism contributing to organ dysfunction in sepsis. Crit Care Clin, 2001, 17: 219。
[104] Jérome Larche, Steve Lancel, Sidi Mohamed Hassoun, Raphael Favory, Brigitte Decoster, Philippe Marchetti, Claude Chopin, Remi Neviere. Inhibition of Mitochondrial Permeability Transition Prevents Sepsis-Induced Myocardial Dysfunction and Mortality. J. Am. Coll. Cardiol, 2006, 48: 377-385.
[105] J Barroso-Aranda, GW Schmid-Schonbein, BW Zweifach,RL Engler. Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock. Circulation Research, 1988, 63: 437-447.
[106] JL Zhao, YJ Yang, CJ Cui, SJ You, YJ Wu, RL Gao. Different effects of adenosine and calcium channel blockade on myocardial no-reflow after acute myocardial infarction and reperfusion. Cardiovasc Drugs Ther, 2006,20(3): 167-175.
[107] JL Zhao, YJ Yang, SJ You, ZC Jing, YJ Wu, WX Yang, JL Chen, RL Gao, ZJ Chen. Effect of adenosine on endothelin-1 in the infarcted reflow and no-reflow myocardium of mini-swine. Zhongguo Yi Xue Ke Xue Yuan Xue Bao, 2006, 28(2): 225-229.
[108] JL Zhao, YJ Yang, YJ Wu, ZC Jing, SJ You, WX Yang, L Meng, Y Tian, JL Chen, RL Gao, ZJ Chen. Effects of anti-platelet drugs on myocardial no-reflow after acute myocardial infarction and reperfusion: experiment with mini-swine model. Zhonghua Yi Xue Za Zhi, 2005, 85(31): 2187-2191.
[109] H Macarthur, DM Couri, GH Wilken, TC Westfall, AJ Lechner, GM Matuschak, Z Chen, D Salvemini. Modulation of serum cytokine level by a novel superoxide dismutase mimetic, M40401, in an Escherichia coli model of septic shock: correlation with preserved circulating catecholamines. Crit Care Med, 2003, 31: 237 - 245.
[110] K Takakura, T Taniguchi, I Muramatsu, K Takeuchi, S Fukuda. Modification of alpha1 -adrenoceptors by peroxynitrite as a possible mechanism of systemic hypotension in sepsis. Crit Care Med, 2002, 30(4): 894-899.
[111] Csaba Szabó, Basilia Zingarelli, Andrew L. Salzman. Role of Poly-ADP Ribosyltransferase Activation in the Vascular Contractile and Energetic Failure Elicited by Exogenous and Endogenous Nitric Oxide and Peroxynitrite. Circ. Res, 1996, 78: 1051 - 1063.
[112] Ya-Ching Hsieh, Shaolong Yang, Mashkoor A. Choudhry, Huang-Ping Yu, Kirby I. Bland, Martin G. Schwacha, Irshad H. Chaudry. Flutamide restores cardiac function after trauma-hemorrhage via an estrogen-dependent pathway through upregulation of PGC-1. Am J Physiol Heart Circ Physiol, 2006, 290: H416-423.
[113] Anne Craveiro Br?chner, Palle Toft. Pathophysiology of the systemicinflammatory response after major accidental trauma. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 2009, 17: 43.
[114] Zhao KS. Advances in the study on rheological behavior of leukocyte during severe shock. Chin Med J, 1996, 109: 110.
[115] Dieter Rixen,J ohn H Siegel. Bench-to-bedside review: Oxygen debt and its metabolic correlates as quantifiers of the severity of hemorrhagic and posttraumatic shock. Critical Care, 2005 9: 441-453.
[116]甯交琳,赖西南,葛衡江,王韶亮,莫立稳,王丽丽,朱剑武.控制性低温对创伤失血性休克后早期炎症反应及器官功能的影响.创伤外科杂志, 2007, 27(2): 143-145.
[117]熊申宁,许建宁.雌激素对创伤失血性休克大鼠肝脏功能的影响.江西医学院学报, 2005, 45(6): 51-53.
[118]冯浩淼,黄宗海,黄绪亮,孙英刚,林洪武. L-精氨酸对创伤性休克大鼠的保护作用研究.中国急救医学, 2004, 24(1): 1-3.
[119] T Murata, H Nakazawa, I Mori, Y Ohta, H Yamabayashi. Reperfusion after a two hour period of pulmonary artery occlusion cause pulmonary necrosis. Am Rev Respir Dis, 1992, 146 (4): 1048 - 1053.