高氧液对低压缺氧复合光气中毒急性肺损伤保护作用及相关机理研究
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摘要
光气是一种有毒气体,是塑料、染料、农药等化工产品化学合成过程中的原料,同时也作为军用毒剂被用于战争和恐怖活动中。光气经呼吸道吸入后可引起严重的弥漫性肺水肿,逐渐加重的肺部气体交换功能障碍导致渐进性低氧血症,肺顺应性降低,严重者可发展成为成人呼吸窘迫综合征(ARDS),甚至死亡。高原空气稀薄,降低的大气压导致氧分压低,这是高原环境影响机体各脏器功能的主要因素。高原环境下吸入光气,低压缺氧既可以造成机体一系列异常反应[1],也会加重化学毒物对机体脏器功能的损伤[2]。初入高原人员若发生光气中毒,机体将同时遭受高原缺氧和光气中毒性损伤双重打击。目前,高原低压缺氧的研究报道已较多,但是,尚未见国内外对高原地区光气中毒的研究报道,本研究突破传统呼吸道给氧方法,应用液体携氧方式,探讨高氧医用液体(简称高氧液)对低压缺氧复合光气中毒急性肺损伤的救治作用,为平时和战时高原地区窒息性毒气造成急性肺损伤的治疗提供新的方法和途径。
第一部分高原低压缺氧复合光气中毒急性肺损伤及相关机制研究
目的:本研究通过建立兔高原低压缺氧复合光气中毒急性肺损伤模型,研究低压缺氧复合光气中毒引起的急性肺损伤特点及其相关机理。
方法:健康新西兰大白兔40只,雌雄不拘,随机分为4组(n=10),正常对照组(C组,染毒柜内吸入空气5min,然后将动物置于低压舱内,但不降低舱内空气压力2h);单纯高原低压缺氧组(H组,染毒柜里吸入空气5min,随即放入模拟高原3000m动物低压舱内2h);单纯光气中毒组(P组,染毒柜内吸入光气5min,然后放入模拟高原动物低压舱内常压下2h);低压缺氧复合光气中毒组(HP组,将动物染毒5min后放入模拟高原3000m低压舱内2h)。观察各组动物实验前(T_1)、出染毒柜后即刻(T_2)、出舱后即刻(T_3)、1h(T_4)、6h(T_5)时间点动物呼吸频率、心率、口唇紫绀等一般情况;抽取动脉血,测定动脉血气分析指标,记录动脉血PaO_2并计算氧合指数(PaO_2/FiO_2);测定血液丙二醛(MDA)含量、红细胞超氧化物歧化酶(SOD)活性、肿瘤坏死因子2α( TNF-2α)含量、白介素6(IL-6)含量;观察动物24h内生存时间、死亡率。
结果:(1)、HP组与P组相比生存时间明显减少、死亡率明显升高(P<0.05或P<0.01),两组与H组比较生存时间均减少,有显著性统计学意义,H组无一例死亡。(2)、与C组、H组比较,HP组与P组吸入光气后呼吸频率明显增快、PaO_2及氧合指数呈进行性下降(P<0.05或P<0.01),两组动物在出舱后即刻、1h、6h时间点血浆MDA含量显著升高、SOD活性明显降低、TNF2α含量及IL-6含量均不同程度升高(P<0.05或P<0.01);(3)、在出舱后即刻、1h、6h时间点低氧光气中毒组与单纯光气中毒组比较动物呼吸频率明显增快、PaO_2降低、血浆MDA含量显著升高、SOD活性明显降低(P<0.05或P<0.01),前者在出舱后1h、6h的TNF-2α含量及IL-6含量明显高于后者(P<0.05)。
结论:高原低压缺氧环境下光气中毒明显加重光气中毒肺损伤的程度,可能与机体脂质过氧化反应及炎性反应增强有关。
第二部分高氧液对低压缺氧复合光气中毒急性肺损伤的保护作用及相关机理研究
目的:本研究旨在探讨静脉输注高氧液对兔低压缺氧复合光气中毒急性肺损伤的防治作用及机制。
方法:新西兰大白兔40只随机分为4组(n=10)。低氧光气中毒组(HP组,光气染毒3min后放入高原模拟海拔3000m低压舱内2h,复合损伤后不治疗)、平衡盐对照组(HPB组,染毒后在模拟海拔3000m低压舱内同时静脉输入平衡盐20 mL·kg~(-1))、吸氧治疗组(HPO组,染毒后在低压舱内给予持续面罩吸氧,氧流量为0.3L·min~(-1))、高氧液治疗组(HPH组,染毒后在模拟海拔3000m低压舱内静脉输入高氧液20mL·kg~(-1))。分别在实验前(T_1)、出染毒柜后即刻(T_2)、出舱后即刻(T_3)、1h(T_4)、6h(T_5)时间点观察并记录动物呼吸频率;抽取动脉血,测定动脉血PaO2 ;测定血液MDA含量、SOD活性、TNF2α含量、IL-6含量;6h后颈动脉放血处死动物,开胸取肺,测定肺水含量(LW)、肺系数(L·B~(-1));左肺行支气管肺泡灌洗(BAL),测定支气管肺泡灌洗液(BALF)中MDA含量、谷胱甘肽过氧化物酶(GSH-Px)活性及细胞总数、蛋白含量,取部分肺组织作匀浆,检测肺组织GSH、GSSG含量,部分肺组织留作组织病理学检查。
结果:吸氧治疗或高氧液治疗后,在各时间点呼吸频率明显低于HP、HPB组(P<0.05或P <0.01);两组L·B~(-1)和LW均明显低于HP、HPB组(P <0.05);吸氧治疗(HPO组)与高氧液治疗(HPH组)在出舱后即刻、1h、6h时间点血浆MDA含量降低、SOD活性升高、TNF-2α含量与IL-6含量均降低,与后两组相比较有显著性差异(P <0.05或P <0.01),HPH组与HPO组相比,在出舱后即刻、1h时间点PaO_2明显升高、MDA含量降低、SOD活性升高,有显著性统计学差异(P <0.05);肺组织GSSG含量降低,BALF中MDA及蛋白含量下降、GSH-Px活性升高,有显著性差异(P <0.05或P <0.01);组织病理学检查显示:肉眼可见HP、HPB组兔肺有片状暗红区,气肿、水肿区,镜下见肺泡壁增厚,间质水肿,静脉淤血、大量液体和细胞渗出;吸氧治疗或高氧液治疗兔肺外观无明显大片暗红、水肿区,触之柔软,光镜下静脉淤血、液体渗出亦不明显。
结论:(1)高原低压缺氧复合光气中毒造成的急性肺损伤程度比单纯光气中毒或低压缺氧带来的损伤更为严重,可能与低压缺氧、光气两种因素共同造成的机体脂质过氧化反应及应激性炎症反应有关;(2)静脉输注高氧液20ml·kg~(-1)能够明显减轻低氧复合光气中毒急性肺损伤程度,并降低复合损伤引起的体内脂质过氧化反应及炎性反应,对低压缺氧复合光气中毒造成的急性肺损伤有一定的保护作用。
Phosgene belongs to blackdamp,which may cause toxic pneumonia,diffusive and transudatory pulmonary edema, ARDS and death even. The air becomes thinner in plateau. Hypobaric hypoxia is the main and beginning harmful environmental factor to inhigh altitude. Hypoxia is not only harmful to people but also aggravate toxic symptom. Acute exposure in both high altitude and phosgene will cause acute hybobaric hypoxia and acute phosgene poisoning.At present,it has been reported widely about hybobaric hypoxia but phosgene poisoning in high altitude has not been reported before . Recently, Hyperoxia solution (HOS) is used as an effective way to treat anoxia diseases. This study investigated the effects of HOS on phosgene poisoning and hypobaric hypoxia -induced acute lung injury.
Part 1 Experimental studies on damage effects and investigate mechanism on acute rabbit lung injury induced by phosgene poisoning and hypobaric hypoxia
AIM: To investigate the damage effects and investigate mechanism on acute rabbit lung injury induced by phosgene poisoning and hypobaric hypoxia.
METHODS: 40 New Zealand white rabbits (weight 2.0～2.5kg) were randomly divided into 4 groups(n=10):Control group(group C,with fresh and normal pressure ); Hypobaric hypoxia group(group H,with fresh air for 5 min and exposure to a simulated altitude of 3000 m for 2 hours ); Phosgene poisoning group(group P,exposure to phosgene for 5 min only);Phosgene poisoning and hypobaric hypoxia group(group HP, exposure to phosgene for 5 min and a simulated altitude of 3000 m for 2 hours). Breathing frequency was recorded and blood samples were taken at different time points(T_1,T_2,T_3,T_4,T_5) for the determination of PaO_2, plasma malordialdehyde (MDA) contents , superoxide dismutase(SOD) activity and tumor necrosis factor-α( TNF-2α) contents, interleukin-6(IL-6) . Survival time of each rabbit and death rate was recorded in all groups .
RESULTS: (1) The survival time shorten and death rate increased significantly in group HP in comparison with group H(P<0.05 or P<0.01 ).(2) In group P and HP,breathing rate increased, PaO_2 and oxygenation index decreased significatly than in group H and C. At T_3,T_4,T_5 time point, plasma MDA contents, TNF2αand IL-6 contents increased and SOD activity decreased distinctly in group P and HP comparied with group H and C(P<0.05 or P<0.01).(3)In group HP,breathing rate and MDA cotents increased, PaO_2 and SOD activity decreased significatly(P<0.05或P<0.01)at T_3,T_4,T_5 in comparison with group P. TNF-2αand IL-6 contents raised obviously at T_4,T_5 in group HP than group H(P<0.05).
CONCLUSION:Phosgene poisoning and hypobaric hypoxia result in more serious injury in lung than only phosgene poisoning or hypobaric hypoxia.
Part 2 Experimental studies on Protective effects and investigate mechanism of hyperoxia solution infusion on acute rabbit lung injury induced by phosgene poisoning and hypobaric hypoxia.
AIM: To investigate the protective effect and mechanism of HOS on rabbit with acute lung injury induced by phosgene and hypobaric hypoxia.
METHODS : 40 New Zealand white rabbits (weight 2.0～2.5kg) were randomly divided into 4 groups(n=10):Group HP : with exposure to phosgene for 3 min and a simulated altitude of 3000 m for 2 hours;Group HPB :After exposed to phosgene for 3min ,this group was exposed to a simulated altitude of 3000 m for 2 hours with an infusion of balanced salt solution(BS,20mL·kg~(-1)) in 1h ;Group HPO: After exposed to phosgene for 3min ,this group was exposed to a simulated altitude of 3000 m for 2 hours with continued mask oxygen inhalation (0.3 L·min~(-1)) in 1h; Group HPH: After exposed to phosgene for 3min ,this group was exposed to a simulated altitude of 3000 m for 2 hours with an infusion of HOS (20mL·kg~(-1)) in 1h . Breathing frequency was recorded and blood samples were taken at different time points(T_1,T_2,T_3,T_4,T_5) for the determination of PaO_2, plasma malordialdehyde (MDA) contents , superoxide dismutase(SOD) activity and tumor necrosis factor-α( TNF-2α) contents, interleukin-6(IL-6) . After 6 hours, the chests were opened and lungs removed. The wet left lungs were weight for L·B~(-1), then after lavaging bronchoalveolar with 0.9% salt solution for plasma MDA contents,GSH-Px activity and protein level in bronchoalveolar lavage fluid(BALF), they were placed in an oven at 70 deg C and dried to a constant weight to measure LW. Small piece of left lung was homogenized and analyzed tissue Glutathione (GSH/GSSG) contents. The remaining parts of left lung were collected to observe pathologic changes.
RESULTS: Breathing rate and LW ,L·B~(-1) was significantly lower and PaO_2 was higher in HPH and HPO than in HP and HPB. At T_3,T_4,T_5 time point, plasma MDA contents, TNF2αand IL-6 contents decreased and SOD activity increased distinctly in group HPH and HPO in comparison with group HP and HPB(P<0.05 or P<0.01). In group HPH, MDA contents decreased , PaO_2 and SOD activity increased significantly than in group HPO. MDA contents and protein levels in BALF depressed and GSH-Px activity increased distinctly in group HPH and HPO than in group HPB and HP (P<0.01 or P<0.05). ONCLUSION:(1) More serious injury in lung induced by phosgene and hypobaric hypoxia than simple phosgene poisoning or hypobaric hypoxia.(2) Treatment with HOS shown a protective effect on rabbits with acute lung injury induced by phosgene exposure and hypobaric hypoxia.
第一部分高原低压缺氧复合光气中毒急性肺损伤及相关机制研究
目的:本研究通过建立兔高原低压缺氧复合光气中毒急性肺损伤模型,研究低压缺氧复合光气中毒引起的急性肺损伤特点及其相关机理。
方法:健康新西兰大白兔40只,雌雄不拘,随机分为4组(n=10),正常对照组(C组,染毒柜内吸入空气5min,然后将动物置于低压舱内,但不降低舱内空气压力2h);单纯高原低压缺氧组(H组,染毒柜里吸入空气5min,随即放入模拟高原3000m动物低压舱内2h);单纯光气中毒组(P组,染毒柜内吸入光气5min,然后放入模拟高原动物低压舱内常压下2h);低压缺氧复合光气中毒组(HP组,将动物染毒5min后放入模拟高原3000m低压舱内2h)。观察各组动物实验前(T_1)、出染毒柜后即刻(T_2)、出舱后即刻(T_3)、1h(T_4)、6h(T_5)时间点动物呼吸频率、心率、口唇紫绀等一般情况;抽取动脉血,测定动脉血气分析指标,记录动脉血PaO_2并计算氧合指数(PaO_2/FiO_2);测定血液丙二醛(MDA)含量、红细胞超氧化物歧化酶(SOD)活性、肿瘤坏死因子2α( TNF-2α)含量、白介素6(IL-6)含量;观察动物24h内生存时间、死亡率。
结果:(1)、HP组与P组相比生存时间明显减少、死亡率明显升高(P<0.05或P<0.01),两组与H组比较生存时间均减少,有显著性统计学意义,H组无一例死亡。(2)、与C组、H组比较,HP组与P组吸入光气后呼吸频率明显增快、PaO_2及氧合指数呈进行性下降(P<0.05或P<0.01),两组动物在出舱后即刻、1h、6h时间点血浆MDA含量显著升高、SOD活性明显降低、TNF2α含量及IL-6含量均不同程度升高(P<0.05或P<0.01);(3)、在出舱后即刻、1h、6h时间点低氧光气中毒组与单纯光气中毒组比较动物呼吸频率明显增快、PaO_2降低、血浆MDA含量显著升高、SOD活性明显降低(P<0.05或P<0.01),前者在出舱后1h、6h的TNF-2α含量及IL-6含量明显高于后者(P<0.05)。
结论:高原低压缺氧环境下光气中毒明显加重光气中毒肺损伤的程度,可能与机体脂质过氧化反应及炎性反应增强有关。
第二部分高氧液对低压缺氧复合光气中毒急性肺损伤的保护作用及相关机理研究
目的:本研究旨在探讨静脉输注高氧液对兔低压缺氧复合光气中毒急性肺损伤的防治作用及机制。
方法:新西兰大白兔40只随机分为4组(n=10)。低氧光气中毒组(HP组,光气染毒3min后放入高原模拟海拔3000m低压舱内2h,复合损伤后不治疗)、平衡盐对照组(HPB组,染毒后在模拟海拔3000m低压舱内同时静脉输入平衡盐20 mL·kg~(-1))、吸氧治疗组(HPO组,染毒后在低压舱内给予持续面罩吸氧,氧流量为0.3L·min~(-1))、高氧液治疗组(HPH组,染毒后在模拟海拔3000m低压舱内静脉输入高氧液20mL·kg~(-1))。分别在实验前(T_1)、出染毒柜后即刻(T_2)、出舱后即刻(T_3)、1h(T_4)、6h(T_5)时间点观察并记录动物呼吸频率;抽取动脉血,测定动脉血PaO2 ;测定血液MDA含量、SOD活性、TNF2α含量、IL-6含量;6h后颈动脉放血处死动物,开胸取肺,测定肺水含量(LW)、肺系数(L·B~(-1));左肺行支气管肺泡灌洗(BAL),测定支气管肺泡灌洗液(BALF)中MDA含量、谷胱甘肽过氧化物酶(GSH-Px)活性及细胞总数、蛋白含量,取部分肺组织作匀浆,检测肺组织GSH、GSSG含量,部分肺组织留作组织病理学检查。
结果:吸氧治疗或高氧液治疗后,在各时间点呼吸频率明显低于HP、HPB组(P<0.05或P <0.01);两组L·B~(-1)和LW均明显低于HP、HPB组(P <0.05);吸氧治疗(HPO组)与高氧液治疗(HPH组)在出舱后即刻、1h、6h时间点血浆MDA含量降低、SOD活性升高、TNF-2α含量与IL-6含量均降低,与后两组相比较有显著性差异(P <0.05或P <0.01),HPH组与HPO组相比,在出舱后即刻、1h时间点PaO_2明显升高、MDA含量降低、SOD活性升高,有显著性统计学差异(P <0.05);肺组织GSSG含量降低,BALF中MDA及蛋白含量下降、GSH-Px活性升高,有显著性差异(P <0.05或P <0.01);组织病理学检查显示:肉眼可见HP、HPB组兔肺有片状暗红区,气肿、水肿区,镜下见肺泡壁增厚,间质水肿,静脉淤血、大量液体和细胞渗出;吸氧治疗或高氧液治疗兔肺外观无明显大片暗红、水肿区,触之柔软,光镜下静脉淤血、液体渗出亦不明显。
结论:(1)高原低压缺氧复合光气中毒造成的急性肺损伤程度比单纯光气中毒或低压缺氧带来的损伤更为严重,可能与低压缺氧、光气两种因素共同造成的机体脂质过氧化反应及应激性炎症反应有关;(2)静脉输注高氧液20ml·kg~(-1)能够明显减轻低氧复合光气中毒急性肺损伤程度,并降低复合损伤引起的体内脂质过氧化反应及炎性反应,对低压缺氧复合光气中毒造成的急性肺损伤有一定的保护作用。
Phosgene belongs to blackdamp,which may cause toxic pneumonia,diffusive and transudatory pulmonary edema, ARDS and death even. The air becomes thinner in plateau. Hypobaric hypoxia is the main and beginning harmful environmental factor to inhigh altitude. Hypoxia is not only harmful to people but also aggravate toxic symptom. Acute exposure in both high altitude and phosgene will cause acute hybobaric hypoxia and acute phosgene poisoning.At present,it has been reported widely about hybobaric hypoxia but phosgene poisoning in high altitude has not been reported before . Recently, Hyperoxia solution (HOS) is used as an effective way to treat anoxia diseases. This study investigated the effects of HOS on phosgene poisoning and hypobaric hypoxia -induced acute lung injury.
Part 1 Experimental studies on damage effects and investigate mechanism on acute rabbit lung injury induced by phosgene poisoning and hypobaric hypoxia
AIM: To investigate the damage effects and investigate mechanism on acute rabbit lung injury induced by phosgene poisoning and hypobaric hypoxia.
METHODS: 40 New Zealand white rabbits (weight 2.0～2.5kg) were randomly divided into 4 groups(n=10):Control group(group C,with fresh and normal pressure ); Hypobaric hypoxia group(group H,with fresh air for 5 min and exposure to a simulated altitude of 3000 m for 2 hours ); Phosgene poisoning group(group P,exposure to phosgene for 5 min only);Phosgene poisoning and hypobaric hypoxia group(group HP, exposure to phosgene for 5 min and a simulated altitude of 3000 m for 2 hours). Breathing frequency was recorded and blood samples were taken at different time points(T_1,T_2,T_3,T_4,T_5) for the determination of PaO_2, plasma malordialdehyde (MDA) contents , superoxide dismutase(SOD) activity and tumor necrosis factor-α( TNF-2α) contents, interleukin-6(IL-6) . Survival time of each rabbit and death rate was recorded in all groups .
RESULTS: (1) The survival time shorten and death rate increased significantly in group HP in comparison with group H(P<0.05 or P<0.01 ).(2) In group P and HP,breathing rate increased, PaO_2 and oxygenation index decreased significatly than in group H and C. At T_3,T_4,T_5 time point, plasma MDA contents, TNF2αand IL-6 contents increased and SOD activity decreased distinctly in group P and HP comparied with group H and C(P<0.05 or P<0.01).(3)In group HP,breathing rate and MDA cotents increased, PaO_2 and SOD activity decreased significatly(P<0.05或P<0.01)at T_3,T_4,T_5 in comparison with group P. TNF-2αand IL-6 contents raised obviously at T_4,T_5 in group HP than group H(P<0.05).
CONCLUSION:Phosgene poisoning and hypobaric hypoxia result in more serious injury in lung than only phosgene poisoning or hypobaric hypoxia.
Part 2 Experimental studies on Protective effects and investigate mechanism of hyperoxia solution infusion on acute rabbit lung injury induced by phosgene poisoning and hypobaric hypoxia.
AIM: To investigate the protective effect and mechanism of HOS on rabbit with acute lung injury induced by phosgene and hypobaric hypoxia.
METHODS : 40 New Zealand white rabbits (weight 2.0～2.5kg) were randomly divided into 4 groups(n=10):Group HP : with exposure to phosgene for 3 min and a simulated altitude of 3000 m for 2 hours;Group HPB :After exposed to phosgene for 3min ,this group was exposed to a simulated altitude of 3000 m for 2 hours with an infusion of balanced salt solution(BS,20mL·kg~(-1)) in 1h ;Group HPO: After exposed to phosgene for 3min ,this group was exposed to a simulated altitude of 3000 m for 2 hours with continued mask oxygen inhalation (0.3 L·min~(-1)) in 1h; Group HPH: After exposed to phosgene for 3min ,this group was exposed to a simulated altitude of 3000 m for 2 hours with an infusion of HOS (20mL·kg~(-1)) in 1h . Breathing frequency was recorded and blood samples were taken at different time points(T_1,T_2,T_3,T_4,T_5) for the determination of PaO_2, plasma malordialdehyde (MDA) contents , superoxide dismutase(SOD) activity and tumor necrosis factor-α( TNF-2α) contents, interleukin-6(IL-6) . After 6 hours, the chests were opened and lungs removed. The wet left lungs were weight for L·B~(-1), then after lavaging bronchoalveolar with 0.9% salt solution for plasma MDA contents,GSH-Px activity and protein level in bronchoalveolar lavage fluid(BALF), they were placed in an oven at 70 deg C and dried to a constant weight to measure LW. Small piece of left lung was homogenized and analyzed tissue Glutathione (GSH/GSSG) contents. The remaining parts of left lung were collected to observe pathologic changes.
RESULTS: Breathing rate and LW ,L·B~(-1) was significantly lower and PaO_2 was higher in HPH and HPO than in HP and HPB. At T_3,T_4,T_5 time point, plasma MDA contents, TNF2αand IL-6 contents decreased and SOD activity increased distinctly in group HPH and HPO in comparison with group HP and HPB(P<0.05 or P<0.01). In group HPH, MDA contents decreased , PaO_2 and SOD activity increased significantly than in group HPO. MDA contents and protein levels in BALF depressed and GSH-Px activity increased distinctly in group HPH and HPO than in group HPB and HP (P<0.01 or P<0.05). ONCLUSION:(1) More serious injury in lung induced by phosgene and hypobaric hypoxia than simple phosgene poisoning or hypobaric hypoxia.(2) Treatment with HOS shown a protective effect on rabbits with acute lung injury induced by phosgene exposure and hypobaric hypoxia.
引文
1. Lahiri S, Di-Giulio-C, Roy A. Lessons from chronic intermittent and sustained hypoxia at high altitudes. Respir Physiolo Neurobiol, 2002, 130(3):223-223.
2.董兆君,赵吉青,吴强.模拟高原缺氧复合梭曼中毒脑损伤特点及其救治.卫生毒理学杂志, 1999, 13(3):185-185.
3.董兆君.高原缺氧环境化学毒剂伤的伤情特点.解放军医学杂志, 2008, 33(2):123-125.
4.徐礼鲜,邢军,曹强.高氧液静脉液体给氧在缺血缺氧疾病治疗中的应用.第四军医大学学报, 2000, 21(1):48-49.
5.孙绪德,柴伟,马家海.高氧液对家兔心肌缺血再灌注损伤的保护作用.心脏杂志, 2001, 13(1):24-26.
6.桑韩飞,张英民,徐礼鲜.高氧液预处理对兔脊髓缺血损伤的保护作用及机制.第四军医大学学报, 2003, 24(20):1870-1874.
7.徐瑞芬,徐礼鲜,徐世荣.高氧液对家兔油酸型急性肺损伤的治疗作用.第四军医大学学报, 2003, 24(16):1451-1453.
8.王玲,徐礼鲜,海春旭.高氧液治疗家兔光气中毒急性肺损伤.第四军医大学学报. 2003, 24(13):1186-1188.
9.张惠,徐礼鲜,张晓峰.高氧液口服和静脉治疗高原低氧血症.第四军医大学学报, 2003, 24(17):1598-1600.
10.海春旭.急性光气中毒机制与防护研究进展.毒理学杂志. 2007, 21(5):371-373.
11. Diller WF. Pathogenesis of phosgene poisoning. Toxicol Ind Health, 1985, 1: 7-15.
12. Guo YL. Kennedy TP, Michael JR. Mechanism of phosgene-induced lungtoxicity: role of arachidonate mediators. J Appl Physiol, 1990, 69: 1615-1622.
13. Kenney TP, Michael JR, Hoidal JR,et al. Dibutyryl camp, aminophylline, and B-adrenergic agonists protect against pulmonary edema caused by phosgene. J Appl physiol, 1989, 67: 2542-2552.
14. Wells BA. Phosgene. A practitioner’s viewpoint. Toxicol Ind Health, 1985, 81-92.
15.徐明之,尉康岭,倪为民.急性光气中毒研究进展.中华劳动卫生职业病杂志, 1998, 16(4):254-255.
16.李文丽,海春旭,梁欣.光气致小鼠肺水肿及肝脏过氧化损伤的实验研究.卫生毒理学杂志, 2004, 18(1):10-12.
17.张晓迪,海春旭,李文丽等.维生素E与硫辛酸对光气损伤的抗氧化作用探讨.癌变·畸变·突变, 2004, 16 (3):132-133.
18. Qin XJ , Li YN , Liang X. The dysfunction of ATPases due to impaired mitochondrial respiration in p hosgene - induced pulmonary edema. Biochem Biophys Res Commun, 2008, 367(1):150-155.
19.海春旭,陈宏莉.光气急性中毒机制的深入研究.癌变畸变突变, 2010, 22(5):401-403.
20. Li WL , Hai CX, Liang X. Apoptosis of ATI I cells in mice induced by phosgene. Inhal Toxicol, 2006, 18(1):71-77.
21. Murray JF, Mathay MA, Luce JM, et al. An expended definition of the ARDS. Am Rev Respir, 1998, 138:720-723.
22. Lee WL, Downey GP. Neutrophilactivation and acute lung injury. Curr Opin Crit Care, 2001, 7(1):17-20.
23. Fein AM, Calalang Colucci MG. Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock. Crit Care Clin, 2000, 16(2): 289-371.
24. Downey GP, Dong Q, Kruger J. Regulation of neutrophil activation in acute lung injury. Chest, 1999, 116:46-54.
25. Strieter RM, Kunkel SL, Keane MP. Chemokines in lung injury. Chest, 1999, 116:103-110.
26. Fujishima S, Aikawa N. Neutrophil mediated tissue injury and its modulation. Intensive Care Med, 1995, 21(3):277-285.
27.仇万山,景华.体外循环与炎性肺损伤.医学研究生学报, 2001, 14(2):164-168.
28. Shames BD, Zallen GS, Mcintyre RC. Chemokinesas mediators of diseases related to surgical conditions. Shock, 2000, 14(1):17-22.
29. Doerschuk CM, Mizgerd JP, Kubo H. Adhension molecules and cellular biomechanical changes in acute lung injury. Chest, 1999, 166 (suppl1):37-43.
30. Akira S, Hirano T, Taga T. Biology of multifunctional cytokines: IL-6 and related molecules IL-1 and TNF. FASEB J, 1990, 4:2860-2863.
31. Feurstein G, Rabinovici R. Importance of interleukin-8 and chemokines in organ injury and shock. Crit Care Med, 1994, 22:550-553.
32. Camussi G, Montructhio G, Dominioni L. Setpic shock the unraveling of molecular mechanisms. Nephrol Diol Transplant, 1995, 10:1808-1813.
33. Wheeler AP, Jesmack G, Brigham KL. Tumor necrosis factor’s effects on lung mechanics, gas exchange and airway reactivating in sheep. J Appl Physiol, 1990, 68(6):2542-2546.
34. Hohlfeldf T, Klemmp, Thiemermann C. The contribution of tumor necrosis factor-alpha and endothelin-1 to the increase of coronary resistance in hearts from rats treated with endotoxin. Br J Pharmacol, 1995, 116(8):3309-3315.
35. Fahey T J, Yoshioka T, Shires GT. The role of tumor necrosis factor and nitric oxide in the acute cardiovascular response to endotoxin. Ann Surg,1996, 223:(1):63-69.
36. Wells BA, Phosgene. A practitioner’s viewpoint. Toxicol Ind Health, 1985, 1:81-92.
37.王莹.急性光气中毒的临床表现与抢救.化工劳动卫生通讯, 1995, 12:20-23.
38.钟南山,府军,朱元玉.现代呼吸病进展.中国医药科技出版社, 1994, 536-538.
39. Dosek A, Ohno H, Acs Z. High altitude and oxidative stress. Respir Physiol Neurobiol, 2007, 158(2-3):128-131.
40. Vats P, Singh VK, Singh SN. High altitude induced anorexia: effect of changes in leptin and oxidative stress levels. Nutr Neurosci, 2007, 10(5-6):243-249.
41. Khan S, O'Brien PJ. Modulating hypoxia-induced hepatocyte injury by affecting intracellular redox state. Biochim Biophys Acta, 1995, 1269(2):153-161.
42. Serrano J, Encinas JM, Salas E. Hypobaric hypoxia modifies constitutive nitric oxide synthase activity and protein nitration in the rat cerebellum. Brain Res, 2003, 976(1):109-119.
43. Radak Z, Lee K, Choi W. Oxidative stress induced by intermittent exposure at a simulated altitude of 4000 m decreases mitochondrial superoxide dismutase content in soleus muscle of rats. Eur J Appl Physiol Occup Physiol, 1994, 69(5):392-395.
44. Nakanishi K, Tajima F, Nakamura A. Effects of hypobaric hypoxia on antioxidant enzymes in rats. J Physiol, 1995, 489(3):869-876.
45. Ilavazhagan G, Bansal A, Prasad Dl. Effect of vitamin E supplementation on hypoxia-induced oxidative damage in male albino rats. Aviat Space Environ Med, 2001, 72(10):899-903.
46. Pfeiffer JM, Askew EW, Roberts DE. Effect of antioxidant supplementation on urine and blood markers of oxidative stress during extended moderate-altitude training. Wilderness Environ Med, 1999, 10(2):66-74.
47. Schmidt MC, Askew EW, Roberts DE. Oxidative stress in humans training in a cold, moderate altitude environment and their response to a phytochemical antioxidant supplement. Wilderness Environ Med, 2002, 13(2):94-105.
48. Shrivastava K, Shukla D, Bansal A. Neuroprotective effect of cobalt chloride on hypobaric hypoxia-induced oxidative stress. Neurochem Int, 2008, 52(3):368-375.
49. Bailey DM, Kleger GR, Holzgraefe M. Pathophysiological significance of peroxidative stress, neuronal damage, and membrane permeability in acute mountain sickness. J Appl Physiol, 2004, 96(4):1459-463.
50. Subudhi AW, Jacobs KA, Hagobian TA. Antioxidant supplementation does not attenuate oxidative stress at high altitude. Aviat Space Environ Med, 2004, 75(10):881-888.
51. Gonzalez NC, Wood JG. Leukocyte-endothelial interactions in environmental hypoxia. Adv Exp Med Biol, 2001, 502:39-60.
52. Nakanishi K, Tajima F, Nakamura A. Effects of hypobaric hypoxia on antioxidant enzymes in rats. J Physiol, 489(3):869-876.
53. Maiti P, Singh SB, Sharma AK. Hypobaric hypoxia induces oxidative stress in rat brain. Neurochem Int, 2006, 49(8):709-716.
54. Kumar D, Bansal A, Thomas P. Biochemical and immunological changes on oral glutamate feeding in male albino rats. Int J Biometeorol, 1999, 42(4):201-204.
55. Radak Z, Taylor AW, Ohno H. Adaptation to exercise-induced oxidative stress: from muscle to brain. Exerc Immunol Rev, 2001, 7:90-107.
56. Joanny P, Steinberg J, Robach Pl. Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise. Resuscitation, 2001, 49(3):307-314.
57. Moller P, Loft S, Lundby C. Acute hypoxia and hypoxic exercise induce DNA strand breaks and oxidative DNA damage in humans. FASEB J, 2001, 15(7):1181-1186.
58. Vij AG, Dutta R, Satija NK. Acclimatization to oxidative stress at high altitude. High Alt Med Biol, 2005, 6(4):301-310.
59. Wilber RL, Holm PL, Morris DM. Effect of FIO2 on oxidative stress during interval training at moderate altitude. Med Sci Sports Exerc, 2004, 36(11):1888-1894.
60.钱令嘉.低氧适应相关基因及其研究策略的思考.中国基础科学, 2001, (9):10-15.
61.高钰琪,黄缄,黄庆愿.高原军事医学基础研究进展.西南国防医药, 2003, 13(5):561-564.
62. Schoene RB. Illnesses at high altitude. Chest, 2008, 134(2):402-416.
63.王海涛,方以群.急性缺氧对机体机能影响的研究进展.海军医学杂志, 2006, 27(2):163-166.
64. West JB. The physiologic basis of high-altitude diseases. Ann Intern Med, 2004, 141(10):789-800.
65. Qiao R,Emenuel C,Sime F. Ventilatory response to moderate hypoxia in peruvian high-and low-landers. Chin J Physio1 Sci, 1995, l1:37-45.
66. Tsukimoto K, Yoshimura N, Ichioka M, Tojo N,Miyazato I, Marumo F. Protein, cell and LTB4 concentrations of lung edema fluid produced by high capillary pressures in rabbit. J Appl Physiol, 1994, 76:321-321.
67. Lalley JG, Kavanagh BP. Hypocapnia.N En J Med, 2002, 34(7):43-53.
68. Moundgil R, Michelakis ED, Archer SL. Hypoxic pulmonary vasoconstriction. J Appl Physiol, 2005, 98:390-403.
69. M aggiorini M. H igh altitude-induced Cardiovasc Res, 2006, 72:41-50.
70. Schoene RB, Swenson ER, Pizzo CJ. The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema.J Appl Physiol, 1988, 64:2605-2613.
71. West JB, Mathieu-Costello O. High altitude pulmonary edema is caused by stress failure of pulmonary capillaries. Int J Sports Med, 1992, 13:S54-58.
72. Tsukimoto K,Yoshimura N,Ichioka M. Protein, cell and LTB4 concentrations of lung edema fluid produced by high capillary pressures in rabbit. J Appl Physiol, 1994, 76:321-321.
73. Droma Y, Hayano T, Takabayashi Y. Endothelin-1 and interleukin-8 in high altitude pulmonary edema. Eur Respir J, 1996, 9:1947-1947.
74. Swenson ER, Maggiorini M, Mongovin S. Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. JAMA, 2002, 287(17):2228-2228.
75. Van Osta A, Moraine JJ, Melot C. Effects of high altitude exposure on cerebral hemodynamics in normal subjects. Stroke, 2005, 36:557-560.
76. Hackett PH, Roach RC. High altitude cerebral edema. High Ah M ed Biol, 2004, 5:136-146.
77. Kallenberg K, Bailey DM, Christ S. Magnetic resonance imaging evidence of cytotoxic cerebral edema in acute mountain sickness. J Cereb Blood Flow M etab, 2007, 27:1064-1071.
78.刘勇,程天民,董兆君.缺氧条件下梭曼中毒大鼠心脏功能变化研究.解放军预防医学杂志, 1999, 17(6):409-409.
79.岳茂兴.窒息性气体中毒的机制及特点和现场急救原则.中国全科医学, 2003, 6:150-152.
80.叶华虎,袁菊芳,王艳静.缺氧环境下氰化物的毒性变化及42DMAP的解毒效果研究.高原医学杂志, 2006, ,16(1):1.
81.唐禾,蔡颖,王涛.缺氧复合NaCN中毒对大鼠心功能的影响.解放军医学杂志, 2008, 33(2):126.
82.魏相德.高原神经毒中毒研究概况.卫生毒理学杂志, 1997, 11(1):23-24.
83.刘勇,程天民,董兆君.缺氧条件下梭曼中毒大鼠心脏功能变化研究.解放军预防医学杂志, 1999, 17(6):409.
84.蔡颖,唐禾,刘辉.缺氧复合氰化钠中毒对大鼠BALF和肺组织磷脂含量的影响.解放军医学杂志, 2008, 33(2):129.
85.张晓声,高诚.自体血紫外线照射后再输入的发展.国外医学输血及血液学分册, 1988, 11(4):269-270.
86.孙星炯,黄彬.某些血液理疗法的临床应用与展望.国外医学物理医学与康复学分册, 2000, 20(2):69-71.
87. Lianin II. Blood ozone in the treatment of patients with progressive pulmonary tuberculosis concurrent with diabetes mellitus. Probl Tuberk, 1988, 1:30-33.
88. Bocci V. Does ozone therapy normalize the cellular redox balance Implications for therapy of human immunodeficiency virus infectionand several other diseases. Med Hypotheses, 1996, 46(2):150-154.
89.徐礼鲜,孙永华.静脉液体供氧新方法的临床应用.第一版.北京:中华电子音像出版社, 2004, 1-154.
90.徐礼鲜,刑军,曹强.高氧液静脉液体给氧在缺血缺氧疾病治疗中的应用.第四军医大学学报, 2003, 24(13):6-7.
91.徐礼鲜,吴利平,张惠.高氧液提高乏氧血氧含量及相关基础研究.中国药理学通报, 2002, 18(5):560-562.
92.杨艳霞,张萍,范秀玲.高氧溶液治疗新生儿缺氧缺血性脑病的疗效观察及护理体会.医学信息, 2006, 19(9):1534-1534.
93. Peralta C, Leon OS, Xaus C. Protective effect of ozone treatment on the injury associated with hepatic ischemia-reperfusion: antioxidant-prooxidant balance. Free Radic Res, 1999, 31(3):191-196.
94. Borrego A, Zamora ZB, Gonzalez R. Protection by ozone preconditioning is mediated by the antioxidant system in cisplatin-induced nephrotoxicity in rats. Mediators Inflamm, 2004, 13(1):13-19.
95.孙绪德,柴伟,张贵和.高氧液在抢救重度失血性休克中的临床应用.临床麻醉学杂志, 2003, 19(6):346-347.
96.何清,许诚,王松.静脉输氧技术治疗感染性疾病严重低氧血症的探讨.中国危重病急救医学, 2004, 16(5):284-286.
97.兰志宏,赖初波.急性一氧化碳中毒的氧疗进展.华夏医学, 2005,18(2):305-306.
98.王祝峰,陈晓茜,李茂林.高氧液治疗重型颅脑伤90例临床分析.解放军医学杂志, 2003, 28(4):377-377.
99.陈箭,陈卫,刘佑云.高氧液对心脑血管疾病疗效的观察.中国自然医学杂志, 2005, 7(1):49-50.
100.杨艳霞,张萍,范秀玲.高氧溶液治疗新生儿缺氧缺血性脑病的疗效观察及护理体会.医学信息, 2006, 19(9):1534-1534.
101.时兢,蔡亚萍,周淑芳.静脉输注高氧液对急性呼吸窘迫综合征的治疗作用.现代诊断与治疗, 2005, 16(3):173-174.
102.姜荣明,龚建新.自由基与常见高原病.铁道劳动安全卫生与环保, 2003, 30(2):103-104.
103.Xu LX, Xing J, Chao Q, Zhao DH. Therapentic effect of hyperoxia solution on anoxic diease. J Fourgh Mil Med Univ, 2001, 22(4):7-9.
104.樊军,刘毅.细胞凋亡与低氧性肺损伤的研究进展.临床军医杂志, 2007, 5(4):617-620.
105.Hackett PH, Yarnell PR, Hill R. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. J Am Med Ass, 1998, 280:1920-1925.
106.Kim BC, Kim HT, Mamura M. Tumor necrosis factor induces apoptosis in hepatoma cells by increasing Ca2+ release from the endoplasmic reticulum and suppressing Bcl-2 expression. Journal of Biological Chemistry, 2002, 277(35):31381-31389.
107.Giunta R, Coppola A, Luongo C. Ozonized autohemotransfusion improves hemorheological parameters and oxygen delivery to tissues in patients with peripheral occlusive arterial disease. Ann Hematol, 2001, 80(12):745-748.
108.Zhao H, Gao CJ, Zhang H. Investigations on physiological basis and clinical applications of hyperoxia solution. SAARC J Anaesth, 2008, 1(2):149-155.
2.董兆君,赵吉青,吴强.模拟高原缺氧复合梭曼中毒脑损伤特点及其救治.卫生毒理学杂志, 1999, 13(3):185-185.
3.董兆君.高原缺氧环境化学毒剂伤的伤情特点.解放军医学杂志, 2008, 33(2):123-125.
4.徐礼鲜,邢军,曹强.高氧液静脉液体给氧在缺血缺氧疾病治疗中的应用.第四军医大学学报, 2000, 21(1):48-49.
5.孙绪德,柴伟,马家海.高氧液对家兔心肌缺血再灌注损伤的保护作用.心脏杂志, 2001, 13(1):24-26.
6.桑韩飞,张英民,徐礼鲜.高氧液预处理对兔脊髓缺血损伤的保护作用及机制.第四军医大学学报, 2003, 24(20):1870-1874.
7.徐瑞芬,徐礼鲜,徐世荣.高氧液对家兔油酸型急性肺损伤的治疗作用.第四军医大学学报, 2003, 24(16):1451-1453.
8.王玲,徐礼鲜,海春旭.高氧液治疗家兔光气中毒急性肺损伤.第四军医大学学报. 2003, 24(13):1186-1188.
9.张惠,徐礼鲜,张晓峰.高氧液口服和静脉治疗高原低氧血症.第四军医大学学报, 2003, 24(17):1598-1600.
10.海春旭.急性光气中毒机制与防护研究进展.毒理学杂志. 2007, 21(5):371-373.
11. Diller WF. Pathogenesis of phosgene poisoning. Toxicol Ind Health, 1985, 1: 7-15.
12. Guo YL. Kennedy TP, Michael JR. Mechanism of phosgene-induced lungtoxicity: role of arachidonate mediators. J Appl Physiol, 1990, 69: 1615-1622.
13. Kenney TP, Michael JR, Hoidal JR,et al. Dibutyryl camp, aminophylline, and B-adrenergic agonists protect against pulmonary edema caused by phosgene. J Appl physiol, 1989, 67: 2542-2552.
14. Wells BA. Phosgene. A practitioner’s viewpoint. Toxicol Ind Health, 1985, 81-92.
15.徐明之,尉康岭,倪为民.急性光气中毒研究进展.中华劳动卫生职业病杂志, 1998, 16(4):254-255.
16.李文丽,海春旭,梁欣.光气致小鼠肺水肿及肝脏过氧化损伤的实验研究.卫生毒理学杂志, 2004, 18(1):10-12.
17.张晓迪,海春旭,李文丽等.维生素E与硫辛酸对光气损伤的抗氧化作用探讨.癌变·畸变·突变, 2004, 16 (3):132-133.
18. Qin XJ , Li YN , Liang X. The dysfunction of ATPases due to impaired mitochondrial respiration in p hosgene - induced pulmonary edema. Biochem Biophys Res Commun, 2008, 367(1):150-155.
19.海春旭,陈宏莉.光气急性中毒机制的深入研究.癌变畸变突变, 2010, 22(5):401-403.
20. Li WL , Hai CX, Liang X. Apoptosis of ATI I cells in mice induced by phosgene. Inhal Toxicol, 2006, 18(1):71-77.
21. Murray JF, Mathay MA, Luce JM, et al. An expended definition of the ARDS. Am Rev Respir, 1998, 138:720-723.
22. Lee WL, Downey GP. Neutrophilactivation and acute lung injury. Curr Opin Crit Care, 2001, 7(1):17-20.
23. Fein AM, Calalang Colucci MG. Acute lung injury and acute respiratory distress syndrome in sepsis and septic shock. Crit Care Clin, 2000, 16(2): 289-371.
24. Downey GP, Dong Q, Kruger J. Regulation of neutrophil activation in acute lung injury. Chest, 1999, 116:46-54.
25. Strieter RM, Kunkel SL, Keane MP. Chemokines in lung injury. Chest, 1999, 116:103-110.
26. Fujishima S, Aikawa N. Neutrophil mediated tissue injury and its modulation. Intensive Care Med, 1995, 21(3):277-285.
27.仇万山,景华.体外循环与炎性肺损伤.医学研究生学报, 2001, 14(2):164-168.
28. Shames BD, Zallen GS, Mcintyre RC. Chemokinesas mediators of diseases related to surgical conditions. Shock, 2000, 14(1):17-22.
29. Doerschuk CM, Mizgerd JP, Kubo H. Adhension molecules and cellular biomechanical changes in acute lung injury. Chest, 1999, 166 (suppl1):37-43.
30. Akira S, Hirano T, Taga T. Biology of multifunctional cytokines: IL-6 and related molecules IL-1 and TNF. FASEB J, 1990, 4:2860-2863.
31. Feurstein G, Rabinovici R. Importance of interleukin-8 and chemokines in organ injury and shock. Crit Care Med, 1994, 22:550-553.
32. Camussi G, Montructhio G, Dominioni L. Setpic shock the unraveling of molecular mechanisms. Nephrol Diol Transplant, 1995, 10:1808-1813.
33. Wheeler AP, Jesmack G, Brigham KL. Tumor necrosis factor’s effects on lung mechanics, gas exchange and airway reactivating in sheep. J Appl Physiol, 1990, 68(6):2542-2546.
34. Hohlfeldf T, Klemmp, Thiemermann C. The contribution of tumor necrosis factor-alpha and endothelin-1 to the increase of coronary resistance in hearts from rats treated with endotoxin. Br J Pharmacol, 1995, 116(8):3309-3315.
35. Fahey T J, Yoshioka T, Shires GT. The role of tumor necrosis factor and nitric oxide in the acute cardiovascular response to endotoxin. Ann Surg,1996, 223:(1):63-69.
36. Wells BA, Phosgene. A practitioner’s viewpoint. Toxicol Ind Health, 1985, 1:81-92.
37.王莹.急性光气中毒的临床表现与抢救.化工劳动卫生通讯, 1995, 12:20-23.
38.钟南山,府军,朱元玉.现代呼吸病进展.中国医药科技出版社, 1994, 536-538.
39. Dosek A, Ohno H, Acs Z. High altitude and oxidative stress. Respir Physiol Neurobiol, 2007, 158(2-3):128-131.
40. Vats P, Singh VK, Singh SN. High altitude induced anorexia: effect of changes in leptin and oxidative stress levels. Nutr Neurosci, 2007, 10(5-6):243-249.
41. Khan S, O'Brien PJ. Modulating hypoxia-induced hepatocyte injury by affecting intracellular redox state. Biochim Biophys Acta, 1995, 1269(2):153-161.
42. Serrano J, Encinas JM, Salas E. Hypobaric hypoxia modifies constitutive nitric oxide synthase activity and protein nitration in the rat cerebellum. Brain Res, 2003, 976(1):109-119.
43. Radak Z, Lee K, Choi W. Oxidative stress induced by intermittent exposure at a simulated altitude of 4000 m decreases mitochondrial superoxide dismutase content in soleus muscle of rats. Eur J Appl Physiol Occup Physiol, 1994, 69(5):392-395.
44. Nakanishi K, Tajima F, Nakamura A. Effects of hypobaric hypoxia on antioxidant enzymes in rats. J Physiol, 1995, 489(3):869-876.
45. Ilavazhagan G, Bansal A, Prasad Dl. Effect of vitamin E supplementation on hypoxia-induced oxidative damage in male albino rats. Aviat Space Environ Med, 2001, 72(10):899-903.
46. Pfeiffer JM, Askew EW, Roberts DE. Effect of antioxidant supplementation on urine and blood markers of oxidative stress during extended moderate-altitude training. Wilderness Environ Med, 1999, 10(2):66-74.
47. Schmidt MC, Askew EW, Roberts DE. Oxidative stress in humans training in a cold, moderate altitude environment and their response to a phytochemical antioxidant supplement. Wilderness Environ Med, 2002, 13(2):94-105.
48. Shrivastava K, Shukla D, Bansal A. Neuroprotective effect of cobalt chloride on hypobaric hypoxia-induced oxidative stress. Neurochem Int, 2008, 52(3):368-375.
49. Bailey DM, Kleger GR, Holzgraefe M. Pathophysiological significance of peroxidative stress, neuronal damage, and membrane permeability in acute mountain sickness. J Appl Physiol, 2004, 96(4):1459-463.
50. Subudhi AW, Jacobs KA, Hagobian TA. Antioxidant supplementation does not attenuate oxidative stress at high altitude. Aviat Space Environ Med, 2004, 75(10):881-888.
51. Gonzalez NC, Wood JG. Leukocyte-endothelial interactions in environmental hypoxia. Adv Exp Med Biol, 2001, 502:39-60.
52. Nakanishi K, Tajima F, Nakamura A. Effects of hypobaric hypoxia on antioxidant enzymes in rats. J Physiol, 489(3):869-876.
53. Maiti P, Singh SB, Sharma AK. Hypobaric hypoxia induces oxidative stress in rat brain. Neurochem Int, 2006, 49(8):709-716.
54. Kumar D, Bansal A, Thomas P. Biochemical and immunological changes on oral glutamate feeding in male albino rats. Int J Biometeorol, 1999, 42(4):201-204.
55. Radak Z, Taylor AW, Ohno H. Adaptation to exercise-induced oxidative stress: from muscle to brain. Exerc Immunol Rev, 2001, 7:90-107.
56. Joanny P, Steinberg J, Robach Pl. Operation Everest III (Comex'97): the effect of simulated sever hypobaric hypoxia on lipid peroxidation and antioxidant defence systems in human blood at rest and after maximal exercise. Resuscitation, 2001, 49(3):307-314.
57. Moller P, Loft S, Lundby C. Acute hypoxia and hypoxic exercise induce DNA strand breaks and oxidative DNA damage in humans. FASEB J, 2001, 15(7):1181-1186.
58. Vij AG, Dutta R, Satija NK. Acclimatization to oxidative stress at high altitude. High Alt Med Biol, 2005, 6(4):301-310.
59. Wilber RL, Holm PL, Morris DM. Effect of FIO2 on oxidative stress during interval training at moderate altitude. Med Sci Sports Exerc, 2004, 36(11):1888-1894.
60.钱令嘉.低氧适应相关基因及其研究策略的思考.中国基础科学, 2001, (9):10-15.
61.高钰琪,黄缄,黄庆愿.高原军事医学基础研究进展.西南国防医药, 2003, 13(5):561-564.
62. Schoene RB. Illnesses at high altitude. Chest, 2008, 134(2):402-416.
63.王海涛,方以群.急性缺氧对机体机能影响的研究进展.海军医学杂志, 2006, 27(2):163-166.
64. West JB. The physiologic basis of high-altitude diseases. Ann Intern Med, 2004, 141(10):789-800.
65. Qiao R,Emenuel C,Sime F. Ventilatory response to moderate hypoxia in peruvian high-and low-landers. Chin J Physio1 Sci, 1995, l1:37-45.
66. Tsukimoto K, Yoshimura N, Ichioka M, Tojo N,Miyazato I, Marumo F. Protein, cell and LTB4 concentrations of lung edema fluid produced by high capillary pressures in rabbit. J Appl Physiol, 1994, 76:321-321.
67. Lalley JG, Kavanagh BP. Hypocapnia.N En J Med, 2002, 34(7):43-53.
68. Moundgil R, Michelakis ED, Archer SL. Hypoxic pulmonary vasoconstriction. J Appl Physiol, 2005, 98:390-403.
69. M aggiorini M. H igh altitude-induced Cardiovasc Res, 2006, 72:41-50.
70. Schoene RB, Swenson ER, Pizzo CJ. The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema.J Appl Physiol, 1988, 64:2605-2613.
71. West JB, Mathieu-Costello O. High altitude pulmonary edema is caused by stress failure of pulmonary capillaries. Int J Sports Med, 1992, 13:S54-58.
72. Tsukimoto K,Yoshimura N,Ichioka M. Protein, cell and LTB4 concentrations of lung edema fluid produced by high capillary pressures in rabbit. J Appl Physiol, 1994, 76:321-321.
73. Droma Y, Hayano T, Takabayashi Y. Endothelin-1 and interleukin-8 in high altitude pulmonary edema. Eur Respir J, 1996, 9:1947-1947.
74. Swenson ER, Maggiorini M, Mongovin S. Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. JAMA, 2002, 287(17):2228-2228.
75. Van Osta A, Moraine JJ, Melot C. Effects of high altitude exposure on cerebral hemodynamics in normal subjects. Stroke, 2005, 36:557-560.
76. Hackett PH, Roach RC. High altitude cerebral edema. High Ah M ed Biol, 2004, 5:136-146.
77. Kallenberg K, Bailey DM, Christ S. Magnetic resonance imaging evidence of cytotoxic cerebral edema in acute mountain sickness. J Cereb Blood Flow M etab, 2007, 27:1064-1071.
78.刘勇,程天民,董兆君.缺氧条件下梭曼中毒大鼠心脏功能变化研究.解放军预防医学杂志, 1999, 17(6):409-409.
79.岳茂兴.窒息性气体中毒的机制及特点和现场急救原则.中国全科医学, 2003, 6:150-152.
80.叶华虎,袁菊芳,王艳静.缺氧环境下氰化物的毒性变化及42DMAP的解毒效果研究.高原医学杂志, 2006, ,16(1):1.
81.唐禾,蔡颖,王涛.缺氧复合NaCN中毒对大鼠心功能的影响.解放军医学杂志, 2008, 33(2):126.
82.魏相德.高原神经毒中毒研究概况.卫生毒理学杂志, 1997, 11(1):23-24.
83.刘勇,程天民,董兆君.缺氧条件下梭曼中毒大鼠心脏功能变化研究.解放军预防医学杂志, 1999, 17(6):409.
84.蔡颖,唐禾,刘辉.缺氧复合氰化钠中毒对大鼠BALF和肺组织磷脂含量的影响.解放军医学杂志, 2008, 33(2):129.
85.张晓声,高诚.自体血紫外线照射后再输入的发展.国外医学输血及血液学分册, 1988, 11(4):269-270.
86.孙星炯,黄彬.某些血液理疗法的临床应用与展望.国外医学物理医学与康复学分册, 2000, 20(2):69-71.
87. Lianin II. Blood ozone in the treatment of patients with progressive pulmonary tuberculosis concurrent with diabetes mellitus. Probl Tuberk, 1988, 1:30-33.
88. Bocci V. Does ozone therapy normalize the cellular redox balance Implications for therapy of human immunodeficiency virus infectionand several other diseases. Med Hypotheses, 1996, 46(2):150-154.
89.徐礼鲜,孙永华.静脉液体供氧新方法的临床应用.第一版.北京:中华电子音像出版社, 2004, 1-154.
90.徐礼鲜,刑军,曹强.高氧液静脉液体给氧在缺血缺氧疾病治疗中的应用.第四军医大学学报, 2003, 24(13):6-7.
91.徐礼鲜,吴利平,张惠.高氧液提高乏氧血氧含量及相关基础研究.中国药理学通报, 2002, 18(5):560-562.
92.杨艳霞,张萍,范秀玲.高氧溶液治疗新生儿缺氧缺血性脑病的疗效观察及护理体会.医学信息, 2006, 19(9):1534-1534.
93. Peralta C, Leon OS, Xaus C. Protective effect of ozone treatment on the injury associated with hepatic ischemia-reperfusion: antioxidant-prooxidant balance. Free Radic Res, 1999, 31(3):191-196.
94. Borrego A, Zamora ZB, Gonzalez R. Protection by ozone preconditioning is mediated by the antioxidant system in cisplatin-induced nephrotoxicity in rats. Mediators Inflamm, 2004, 13(1):13-19.
95.孙绪德,柴伟,张贵和.高氧液在抢救重度失血性休克中的临床应用.临床麻醉学杂志, 2003, 19(6):346-347.
96.何清,许诚,王松.静脉输氧技术治疗感染性疾病严重低氧血症的探讨.中国危重病急救医学, 2004, 16(5):284-286.
97.兰志宏,赖初波.急性一氧化碳中毒的氧疗进展.华夏医学, 2005,18(2):305-306.
98.王祝峰,陈晓茜,李茂林.高氧液治疗重型颅脑伤90例临床分析.解放军医学杂志, 2003, 28(4):377-377.
99.陈箭,陈卫,刘佑云.高氧液对心脑血管疾病疗效的观察.中国自然医学杂志, 2005, 7(1):49-50.
100.杨艳霞,张萍,范秀玲.高氧溶液治疗新生儿缺氧缺血性脑病的疗效观察及护理体会.医学信息, 2006, 19(9):1534-1534.
101.时兢,蔡亚萍,周淑芳.静脉输注高氧液对急性呼吸窘迫综合征的治疗作用.现代诊断与治疗, 2005, 16(3):173-174.
102.姜荣明,龚建新.自由基与常见高原病.铁道劳动安全卫生与环保, 2003, 30(2):103-104.
103.Xu LX, Xing J, Chao Q, Zhao DH. Therapentic effect of hyperoxia solution on anoxic diease. J Fourgh Mil Med Univ, 2001, 22(4):7-9.
104.樊军,刘毅.细胞凋亡与低氧性肺损伤的研究进展.临床军医杂志, 2007, 5(4):617-620.
105.Hackett PH, Yarnell PR, Hill R. High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. J Am Med Ass, 1998, 280:1920-1925.
106.Kim BC, Kim HT, Mamura M. Tumor necrosis factor induces apoptosis in hepatoma cells by increasing Ca2+ release from the endoplasmic reticulum and suppressing Bcl-2 expression. Journal of Biological Chemistry, 2002, 277(35):31381-31389.
107.Giunta R, Coppola A, Luongo C. Ozonized autohemotransfusion improves hemorheological parameters and oxygen delivery to tissues in patients with peripheral occlusive arterial disease. Ann Hematol, 2001, 80(12):745-748.
108.Zhao H, Gao CJ, Zhang H. Investigations on physiological basis and clinical applications of hyperoxia solution. SAARC J Anaesth, 2008, 1(2):149-155.