舒芬太尼后处理对大鼠肠缺血再灌注时肺组织损伤的影响
|
摘要
目的通过研究舒芬太尼对肠缺血再灌注大鼠肺组织及血清中肿瘤坏死因子-α(TNF-α)和肺组织中核因子-κB(NF-κB)的影响,探讨舒芬太尼后处理对大鼠肠缺血再灌注时肺组织的影响及可能机制,以期为临床提供实验依据。
方法将32只健康成年雄性Wistar大鼠,随机分为4组:假手术组(S组)、肠缺血再灌注组(I/R组)、肠缺血后处理组(I-post组)及1ug/kg舒芬太尼后处理组(SP组)。每组各8只。①假手术组:仅行开腹,分离肠系膜上动脉(SMA)不夹闭;②缺血-再灌注组:采用夹闭肠系膜上动脉60min后再灌注120min的方法制备肠I/R模型;③缺血后处理组:缺血60 min后即刻行3个循环的灌注30 s/阻断30 s,余同I/R组。④舒芬太尼后处理组:将1ug/kg舒芬太尼稀释到0.3ml在再灌注即刻经股静脉用微量注射泵泵入0.1ml/30S,期间间断30s,如此循环3次(共0.3ml),余同I/R组。于再灌注120min时处死8只大鼠。HE染色观察大鼠肺组织病理改变。采用放射免疫法测定血清及肺组织中TNF-α的含量;采用免疫组织化学法测定肺组织中NF-κB表达水平。
结果(1)HE检测病理变化:①S组:未发现明显病理变化,肺泡大小均匀,结构完整,壁薄,未见出血水肿及炎性细胞浸润;②I/R组可见肺泡大小不均,完整性破坏,肺泡腔有蛋白样渗出物,肺泡壁增厚,间隔增宽,肺间质和肺泡水肿,大量炎细胞浸润、充血、出血明显。③I-post组、SP组上述病理变化均较轻,肺泡腔内蛋白渗出减少,肺泡壁增厚、炎细胞浸润减轻(。2)TNF-α、NF-κB检测:与S组相比,其余各组TNF-α增加、NF-κB表达上调( );与I/R组相比,I-post组及SP组NF-κB表达下调、TNF-α减少( P ?0.05);I-post组及SP组比较上述指标差异无统计学意义( )。
结论(1)小肠缺血再灌注可以导致严重的肺损伤。(2)肠缺血再灌注肺损伤机制复杂,其发生和发展可能与TNF-α和NF-κB有关。(3)舒芬太尼后处理对肠缺血再灌注导致的肺损伤有保护作用,可抑制肺组织中NF-κB的表达,减轻大鼠肠缺血再灌注时血清及肺组织中TNF-α的含量。
Objective Research sufentanil on intestinal ischemia-reperfusion rat lung tissue and serum tumor necrosis factor-α(TNF-α) and lung tissue nuclear factor-κB (NF-κB), and investigate the effects of Sufentanil post-conditioning (SP) acute lung injury induced by ischemia-reperfusion in rats and possible mechanisms, In order to provide experimental basis for clinical.
Methods Thirty-two healthy male Wistar rats were randomly divided into four group (n=8): Sham-operation group (S group),I/R group(I/R group),intestinal ischemic Post-conditioning group(I-post group) and 1ug/kg Sufentanil post-conditioning group (SP group).Each group of 8.(1)S group :Superrior mesenteric artery was only isolated but not blocked.(2)I/R group was established by clamping superior mesenteric artery(SMA)for 1 hour and reperfusing for 2 hours.(3) Line immediately after 60 min ischemia and 3 cycles of reperfusion 30 s / block 30 s, more than with the I / R group. (4) The 1ug/kg sufentanil diluted to 0. 3ml immediately after reperfusion through the femoral vein with a syringe pump pump 0.1ml/30S, during the intermittent 30s, so the cycle 3 times (a total of 0.3ml), than with the I / R Group. The animals were killed at 2 h of reperfusion respectively (n=8). HE dyed observe lung tissue pathology changes in rats. TNF-αin the serum and lung tissue were determined using radio-immunifaction method .Expression of NF-κB P65 in the lung tissue was assessed by immunohistichemical method.
Results (1) HE detection pathological changes:①S group: not found significant pathological changes, alveolar size uniform, complete structure, wall thin, did not see the bleeding edema and inflammatory cells infiltrating;②I/R group visible alveolar size is uneven and integrity damage, alveolar exudate of cavity have protein samples, the alveolar wall thickening widened, the interval, interstitial lung and alveolar edema, a lot of inflammatory cell, congestion, bleeding obvious.③I-post group and SP group are lighter the pathological changes, the alveolar lumen protein, the alveolar exudate is reduce thickened wall, inflammatory cell ease.
Compared with the sham-operated control group, serum and lung TNF-a lever was increased significantly in the other groups ( ), and NF-kB p65 protein in the lung was increased (P<0.05). Compared with the I/R group, TNF-αin the serum and lung tissues were decreased significantly following Sulfentanil treatment ( ), and the expression of lung NF-κB was markedly ameliorated (P<0.05).There were no significant difference between I-post group and SP group( ).
Conclusion (1)This study demonstrated that intestinal ischemia-reperfusion l may result in sincerely lung damage.(2) The mechanism of lung injury induced by intestinal ischemia-reperfusion is complicated, and its occurrence and development may be related to TNF-αand NF-KB related.(3) sulfentanil post-conditioning on intestinal ischemia-reperfusion induced lung injury has a protective effect, can inhibit NF-κB in lung tissue expression of rat intestinal ischemia and reperfusion reduce the serum and lung tissue content of TNF-α.
方法将32只健康成年雄性Wistar大鼠,随机分为4组:假手术组(S组)、肠缺血再灌注组(I/R组)、肠缺血后处理组(I-post组)及1ug/kg舒芬太尼后处理组(SP组)。每组各8只。①假手术组:仅行开腹,分离肠系膜上动脉(SMA)不夹闭;②缺血-再灌注组:采用夹闭肠系膜上动脉60min后再灌注120min的方法制备肠I/R模型;③缺血后处理组:缺血60 min后即刻行3个循环的灌注30 s/阻断30 s,余同I/R组。④舒芬太尼后处理组:将1ug/kg舒芬太尼稀释到0.3ml在再灌注即刻经股静脉用微量注射泵泵入0.1ml/30S,期间间断30s,如此循环3次(共0.3ml),余同I/R组。于再灌注120min时处死8只大鼠。HE染色观察大鼠肺组织病理改变。采用放射免疫法测定血清及肺组织中TNF-α的含量;采用免疫组织化学法测定肺组织中NF-κB表达水平。
结果(1)HE检测病理变化:①S组:未发现明显病理变化,肺泡大小均匀,结构完整,壁薄,未见出血水肿及炎性细胞浸润;②I/R组可见肺泡大小不均,完整性破坏,肺泡腔有蛋白样渗出物,肺泡壁增厚,间隔增宽,肺间质和肺泡水肿,大量炎细胞浸润、充血、出血明显。③I-post组、SP组上述病理变化均较轻,肺泡腔内蛋白渗出减少,肺泡壁增厚、炎细胞浸润减轻(。2)TNF-α、NF-κB检测:与S组相比,其余各组TNF-α增加、NF-κB表达上调( );与I/R组相比,I-post组及SP组NF-κB表达下调、TNF-α减少( P ?0.05);I-post组及SP组比较上述指标差异无统计学意义( )。
结论(1)小肠缺血再灌注可以导致严重的肺损伤。(2)肠缺血再灌注肺损伤机制复杂,其发生和发展可能与TNF-α和NF-κB有关。(3)舒芬太尼后处理对肠缺血再灌注导致的肺损伤有保护作用,可抑制肺组织中NF-κB的表达,减轻大鼠肠缺血再灌注时血清及肺组织中TNF-α的含量。
Objective Research sufentanil on intestinal ischemia-reperfusion rat lung tissue and serum tumor necrosis factor-α(TNF-α) and lung tissue nuclear factor-κB (NF-κB), and investigate the effects of Sufentanil post-conditioning (SP) acute lung injury induced by ischemia-reperfusion in rats and possible mechanisms, In order to provide experimental basis for clinical.
Methods Thirty-two healthy male Wistar rats were randomly divided into four group (n=8): Sham-operation group (S group),I/R group(I/R group),intestinal ischemic Post-conditioning group(I-post group) and 1ug/kg Sufentanil post-conditioning group (SP group).Each group of 8.(1)S group :Superrior mesenteric artery was only isolated but not blocked.(2)I/R group was established by clamping superior mesenteric artery(SMA)for 1 hour and reperfusing for 2 hours.(3) Line immediately after 60 min ischemia and 3 cycles of reperfusion 30 s / block 30 s, more than with the I / R group. (4) The 1ug/kg sufentanil diluted to 0. 3ml immediately after reperfusion through the femoral vein with a syringe pump pump 0.1ml/30S, during the intermittent 30s, so the cycle 3 times (a total of 0.3ml), than with the I / R Group. The animals were killed at 2 h of reperfusion respectively (n=8). HE dyed observe lung tissue pathology changes in rats. TNF-αin the serum and lung tissue were determined using radio-immunifaction method .Expression of NF-κB P65 in the lung tissue was assessed by immunohistichemical method.
Results (1) HE detection pathological changes:①S group: not found significant pathological changes, alveolar size uniform, complete structure, wall thin, did not see the bleeding edema and inflammatory cells infiltrating;②I/R group visible alveolar size is uneven and integrity damage, alveolar exudate of cavity have protein samples, the alveolar wall thickening widened, the interval, interstitial lung and alveolar edema, a lot of inflammatory cell, congestion, bleeding obvious.③I-post group and SP group are lighter the pathological changes, the alveolar lumen protein, the alveolar exudate is reduce thickened wall, inflammatory cell ease.
Compared with the sham-operated control group, serum and lung TNF-a lever was increased significantly in the other groups ( ), and NF-kB p65 protein in the lung was increased (P<0.05). Compared with the I/R group, TNF-αin the serum and lung tissues were decreased significantly following Sulfentanil treatment ( ), and the expression of lung NF-κB was markedly ameliorated (P<0.05).There were no significant difference between I-post group and SP group( ).
Conclusion (1)This study demonstrated that intestinal ischemia-reperfusion l may result in sincerely lung damage.(2) The mechanism of lung injury induced by intestinal ischemia-reperfusion is complicated, and its occurrence and development may be related to TNF-αand NF-KB related.(3) sulfentanil post-conditioning on intestinal ischemia-reperfusion induced lung injury has a protective effect, can inhibit NF-κB in lung tissue expression of rat intestinal ischemia and reperfusion reduce the serum and lung tissue content of TNF-α.
引文
[1] Edelman DA, Sugawa C, Lower gadtrointestinal bleeding; a review [J].Surg Endose,2007,21(4):514.
[2]杨延芳,肠缺血再灌注肺损伤信号转导机制.现代医药卫生,2006,22(22):3445-3447.
[3]刘克玄,周军.丙泊酚对大鼠肠缺血再灌注所致肺损伤的保护机制[J].中华胃肠外科杂志,2004,7(4):326.
[4]盛志勇,胡森.多器官功能障碍综合征.北京科学出版社,1999:20-21.[5] BoyleEM, et al. AnnThorac Surg 1997, 63(1): 277-284.
[6] Li C, et al. Am J Physiol 1999; 276(2): H543-H552.
[7] Zou L, Atmwaybi B, Kone B C. et a1.Effects of NF-КB inhibition on mesenteric ischemia-reperfusion injury[J].Am J Physiol Gastr0intest Liver Physicl ,2003,284(4):G713-G721
[8] Tian XF. Yan JH, H YH, et a1. Effect of nuclear factor kappaB on intercellular adhesion molecule 1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/repeffusion in rats[J].World Gastroenterol, 2006, 12(3):388.
[9] Itai T, Tanaka M, Nagata S. Processing of tumor necrosis factor by the membrane bound T-NF-αlpha converting enzyme, but not its truncated soluble form [J]. Eur J Biochem, 2001, 26(8):2074-2082.
[10] CHO JE,KIM JE, et al. Epidural sufentanil provides better analgesia from 24h after surgery compared with epidural fentanyl in children [J]. Acta Anaesthesiolo Scand,2008, 52(10):1360-1363.
[11] Borgdorff PJ, Lonescuti, Houweling PL, et al. Large-dose intrathecal sufentanil prevents the hormonal stress response during major abdominal surger :a comparison with intravenous sufentanil in a prospective randomized trial[J].Anesth Analg ,2004,99(4):1114-1120.
[12]潘振祥,段立波,张春城.舒芬太尼术后PCEA对细胞因子、皮质醇的影响[J].临床麻醉学杂志,2006,22(11):856-857.
[13] Mallick IH, Yang W, Winslet MC, et al. Ischemia-reperfusion injury of the intestine and protective strategies against injury.Dig Dis Sci.2004;49(9):1359-77.
[14] Yao JH, Zhang XS, Zheng 55, et al. ProPhylaxis with earnosol attenuates liver injury indueed by intestinal isehemia/rePerfusion. World J Gastroenterol.2009; 15(26):3240-3245.
[15] Wu XT, Li JS, Zhao XF, Zhuang W, Feng XL. Modified techniques of hetero-topictotal small intestinal transplantation in rats.World J Gastroente-rol.2002, 8:758-762.
[16] Stallion A, Kou TD, Latifi SQ, et al. Ischemia/reperfusion: a clinically relevant mode of intestinal injury yielding systemic inflammation. J Pediatr Surg.2005, 40(3):470-477.
[17] Hassoun HT, Kone BC, Mercer DW, et al. Post-injury multiple organ failure: the role of the gut. Shock, 2002:15(1):1-10.
[18] Pierro A and Eaton S. Intestinal ischemia reperfusion injury and multisystem organ failure. Semin Pediatr Surg. 2004; 13(1):11-17.
[19] Ware LB, Matthay MA. The acute respiratory distress syndrome .N Engl J Med. 2000; 342(18):1334-1349.
[20] Prakanrattana U, Suksompong S, .ComParision of sufentanil and fentanyl for surgieal repair of congenitalcardiac defects. J Med Assoc Thai, 2002,85(3):807-14.
[21]金昔陆.池志强.阿片受体激动剂舒芬太尼的药理作用和应用.中国现代应用药学杂志,1999,16(1):1-5.
[22] Monk JP, Beresford R, Ward A. Sufentail A Review of its Pharmacological Properties and Therapeutic Use. ADIS Drug Information Services, 1988, Drugs 36:286-313.
[23]黄继汉,黄晓晖,陈志扬.药理试验中动物间和动物与人体间的等效剂量换算.中国临床药理学与治疗学,2004,9(9):1069-72.
[24]张成明,于金玲,张岩.舒芬太尼对家兔急性肺损伤的影响.中国危重病急救医学,2008,20(2):108-110.
[25]刘鲲鹏,孙海涛,薛富善,等.不同剂量的舒芬太尼预处理对大鼠的延迟性心肌保护作用,中华麻醉学杂志,2009,(5);405-408.
[26]张冬梅,常亚恬,徐向辉,等.舒芬太尼预先给药对大鼠心肌缺血再灌注损伤的影响.中华麻醉学杂志, 2008,28(10):932-935.
[27]张冬梅,侯春丽,常亚恬,等.舒芬太尼预处理对缺血再灌注大鼠心肌梗死范围及心肌酶的影响.实用医学杂志,2009,25(15):2430-2433.
[28]李进,袁世荧,丰新民,等.舒芬太尼延迟后处理对兔心肌缺血再灌注损伤的影响,中华麻醉学杂志, 2009, 29(8):692-695.
[29]金利达,林丽娜,王俊等.舒芬太尼预先给药对兔心肌缺血再灌注的影响.中华麻醉学杂志,2008,28(9):855-857.
[30] Zhao ZQ, Corvera JS, Halkos ME, et al.Inhibition of myocardial injury by ischemic post-conditioning during reperfusion: comparison with ischemic pre-conditioning [J] . Am J Physiol Heart Circ Physiol. 2003, 285(2):H 579-H 588.
[31]姚树桐,刘秀华,赵秀梅等.钙调神经磷酸酶的抑制参与大鼠心脏缺血后处理的保护作用[J].中国病理生理杂志,2008,24(12):2289-2294.
[32]姚树桐,刘秀华,汤旭明等.缺血后处理改善脑缺血再灌注大鼠软脑膜微循环[J].中国病理生理杂志,2009,25(3):451-455.
[33]姚树桐,赵秀梅,刘秀华.细胞间黏附分子-1抑制参与大鼠小肠缺血后处理的保护作用[J].中国微循环,2008,12(2):69-72.
[34]毛张凡,杜心灵,孙宗全,夏家红,阿片受体参与大鼠缺血后处理的心肌保护作用,华中科技大学学报(医学版),2007,36(5):601-613.
[35] Venkatapuram S ,Wang C ,Krolikowski JG ,et al .Inhibition of apoptotic protein P53 lowers the threshold of isoflurane induced cardio protection during early reperfusion in rabbits [J].Anesth Analg ,2006,103(6):1400-1405.
[36] Obal D,Rascher K, Favoccia C,et al. Post-conditioning by a short administration of desflurane reduce renal reperfusion injury after differing of ischaenia tines in rats .British J Anaesth,2006,97:783-791.
[37] Chen H, Xing B,Liu X et al .Ischemic postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat[J]. TransplInt , 2007,17(2):71.
[38]姚树桐,李玉珍,刘秀华,等.缺血后处理对小肠缺血-再灌注损伤大鼠肠系膜微循环的影响[J].微循环杂志,2007,17(2):1.
[39]林世清,黄文起,冯霞,等.缺血后处理对兔小肠缺血再灌注损伤的影响.中华麻醉学杂志,2007,27(11): 1042 -1044.
[40]郝志强,王为忠,李孟彬,等.丙酮酸对大鼠小肠缺血再灌注的保护作用[J].中国临床康复,2004,8(2): 276-277.
[41]文斌,屠伟峰,何静等.大鼠全肠道缺血再灌注后肠道组织和肠道外器官损伤的研究实用医学杂志,2003, 19(2):126-128.
[42] Churg A, Dai J, Tai H, et al. Tumor necrosis factor-alpha is central to acute cigarette smo-ke induced inflammation and connective tissue breakdown[J]. Am J Respir Crit Care Med, 2002,16(6):849-854.
[43] Aldonyte R, Jansson L, Piitulainen E, et al. Circulating monocytes from healthy individuals and COPD patients [J]. Respir Res, 2003,4(2):11.
[44]曲敬祥.慢性阻塞性肺疾病患者血清IL-8和TNF-α测定的临床意义[J].山东医药,2007,47(22): 80.
[45] Souza AL , Jr ,Pontes B ,et al .Gut isocheimal/reperfusion activates lung macrphages for tumor necrosis factor and hydrogen peroxide production .J Trauma 2000;49(2);232-2365
[46] Yao YM, Bahrami S,Redl H ,et al.IL-6 release after intestinal ischemia/reperfusion in rats B, et al. Intestinal ischemia/reperfusion induces bronchial hyper reactivity and increases serum TNF-αin rats . Clinics 2006; 61(1);21-28.
[47]张树平,胡涛,栾海云,李庆忠,李淑翠,刘金平;肠缺血再灌注大鼠肺及血液白细胞介素6、白细胞介素8和肿瘤坏死因子变化与辅酶Q的干预,中国组织工程研究与临床康复;2007,11(27),5429-5431.
[48]姚咏明,田惠明,王亚军等.肿瘤坏死因子在肠缺血所致多器官损伤中的作用.中华整形烧伤外科杂志,1994,10;282-284.
[49] Albert S, Baldwin Jr. The NF-κB and IκB proteins: New discoveries and Insights. Annu Rev Immunol, 1996,14:649-681.
[50] Muller JM, Ziegler-Heitbrock HW, Baeuerle PA. Nuclear factor kappa B, amediator of lipopolysaccharide effects. Immunobiol, 1993, 187:233-256.
[51] Woronicz JD, Gao X, Cao Z, et al. IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK.Science, 1997,278:866-869.
[52] Chandrasekar B, Streitmen JE, Colston JT ,et al.Inhibition of nuclear factor kappaB attenuats proinflammatory cytokine and inducible nitric-oxide synthase expressiom in postischemic myocardium.Biochim Biophys Acta, 1998,1406:91-106.
[53] Blackwell TS, Christman JW. The role of nuclear factor-kappa-B in cytokinegene regulation. Am J Resir Cell Mol Biol, 1997,17:3-9.
[54] Bevilacqua MP, Pober JS, Mendrick DL, et al. Identification of an inducible endothelial-leukocyte adhesion molecule. Proc Natl Acad Sci U S A, 1987, 84:9238-9242.
[55] Zwacka RM, Zhang Y, Zhou W, et al.Ischemia/reperfusion injury in the liver of BALB/c miceactivates AP-1and nuclear factor-κB independently of IκB degradation.Hepatology,1998,28:1022-1030.
[1] Edelman DA, Sugawa C, Lower gadtrointestinal bleeding, a review [J]. Surg Endose,2007 ,21(4):514.
[2]杨延芳,肠缺血再灌注肺损伤信号转导机制;现代医药卫生,2006,22(22):3445-3447
[3]刘克玄,周军.丙泊酚对大鼠肠缺血再灌注所致肺损伤的保护机制[J].中华胃肠外科杂志,2004,7(4);326
[4]盛志勇,胡森,多器官功能障碍综合征.北京科学出版社,1999.20-21.
[5] Boyle EM, et al. Ann Thorac Surg 1997; 63(1): 277-284.
[6] Li C, et al. Am J Physiol 1999; 276(2): H543-H552.
[7] Sen R, Baltimore D. Multiple nuclear factors interact with the immunoglobulim enhancer sequences. Cell, 1986,46:705-716.
[8] Albert S, Baldwin Jr. The NF-κB and IκB proteins: New discoveries and Insights. Annu Rev Immunol, 1996,14:649-681.
[9] Muller JM, Ziegler-Heitbrock HW, Baeuerle PA. Nuclear factor kappa B, amediator of lipopolysaccharide effects. Immunobiol, 1993,187:233-256.
[10] Woronicz JD, Gao X ,Cao Z, et al. IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK.Science, 1997,278:866-869.
[11] Chandrasekar B, Streitmen JE, Colston JT ,et al.Inhibition of nuclear factor kappaB attenuats proinflammatory cytokine and inducible nitric-oxide synthase expressiom in postischemic myocardium.Biochim Biophys Acta, 1998,1406:91-106.
[12] Blackwell TS, Christman JW. The role of nuclear factor-kappa-B in cytokinegene regulation. Am J Resir Cell Mol Biol, 1997, 17:3-9.
[13] Bevilacqua MP, Pober JS, Mendrick DL, et al. Identification of an inducible endothelial-leukocyte adhesion molecule. Proc Natl Acad Sci U S A,1987,84:9238-9242.
[14] Zwacka RM, Zhang Y, Zhou W, et al.Ischemia/reperfusion injury in the liver of BALB/c miceactivates AP-1 and nuclear factor-κB independently of IκB degradation.Hepatology,1998,28:1022-1030.
[15] Akira S,Hirano T,Taga T,et al.Biology of multifunctional cytokines:IL-6 related molecules(IL-1 and TNF-α).FASEB J,1990,4:2860-2867.NF-κB.
[16]Arenzana Seidedos F ,Turpin P ,Rodriguez M ,et al. Nuclear localization of IκB promotes active transport of NF -κB from the nucleus to the cytoplasm[J]. J Cell Sci , 1997 ,110 (3) :369 - 378.
[17] Schmidt K N ,Traenckner EB M , Meier B ,et al. Induction of oxidative stress by odadaic acid is required for activation of transcription factor NF–κB[J]. J Biol Chem , 1995 ,270 (45) :27136 - 27142.
[18] Zou L, Attuwaybi B, Kone BC.Effects of NF-Kappa B inhibition on mesenteric ischemia-reperfusion injury [J].Am Physiol ,2003,284(4):G713.
[19] Arenzana-seisdedos F,Turpin P, Rodriguez M,et al.Nuclear localizaion of IkB promotes active transport of NF-KB from the nucleus to the cytoplasm[J].Cell Sei,1997,110(pt3):369.
[20]Yeh KY, et al.Gastroenterology 2000; 118(3): 525-534.
[21]Hassoun H T , Kozar R A , Kone B C ,et al. Intraischemic hypothermia differentially modulates oxidative stress proteins during mesenteric ischemia/ reperfusion[J]. Surgery,2002 ,32 (2) :369 - 376.
[22]Zou L ,Attuwaybi B , Kone BC. Effects of NF - kappaB inhibition on mesenteric ischemia/ reperfusion injury [J] . Am J Physiol ,2003 ,284 (4) : G713-721.
[23]邬善敏,张训臣.肠上皮细胞凋亡与肠缺血损伤及再生修复的试验研究[J].中华急诊医学杂志,2003 ,12 (9) :604- 606.
[24]Ikeda H ,Suzuki Y,Suzuki M ,et al. Apoptosis is a major mode of cell death caused by ischemia and ischemia/ reperfusion injury to the rat intestinal epithelium. Gut ,1998 ,42 :530 - 537.
[25] Noda T, et al. Am J Physiol 1998; 274(2 Pt1): G270-G276.
[26]Gupta RA, et al. J Biol Chem 2001; 276(33): 31059-31066.
[27]李晓鲁,袁志强,彭毅志.重组腺病毒介导的HSP70转染对肠上皮细胞缺氧再复氧损伤的保护作用.中华医学杂志.2002,82(16)1102-1104.
[28] Feinstein DL, et al. J Biol Chem 1996; 271(30): 17224-17232.
[29] Boyle EM, et al. Ann Thorac Surg 1999; 68(5): 1949-1953.
[30]史晓峰,刘敦贵. 1 ,6 -二磷酸果糖在大鼠小肠缺血再灌注损伤中的保护作用[J].中国临床营养杂志, 2003 ,11 (4) :278 - 280.
[31]方天翎,唐朝晖,胡元龙,夏穗生,等.谷氨酰胺对缺血再灌注损伤早期小肠粘膜细胞凋亡的影响[J].中国临床营养杂志,2003 ,11 (1) :40 - 43.
[32]谢伟霖,蒋更如,尤新民等.N-乙酰半胱氨酸对多器官功能障碍综合征大鼠器官的保护作用及其机制上海医学,2009,32(11):987-991.
[33]Anrather J, et al.J Clin Invest 1997; 99(4): 763-772.
[34].Gan H, Ouyang Q, Chen Y , Liang F . The effects of nuclear factor-kappa B p65 antisenseoligonucleotides on expression of proinfl amatory cytokines in lamina propria mononuclear cells from patients with ulcerative colitis. Shengwu Yixue Gongchengxue Zazhi 2003; 20: 268-272
[35]李弼民,吕农华,谢勇等.NF-KB P65反义寡核苷酸对TNBS结肠炎小鼠肠黏膜细胞因子和NF-KB表达的影响.世界华人消化杂志,2008;16(17):1926-1931.
[36]李英华,田晓峰,王真真.NF-KB对肠缺血再灌注肝损伤P-选择素表达和中性粒细胞浸润的作用世界华人消化杂志2006,14(5):486-490.
[37]陈茂松,崔海宁,张克君,等.核因子-κB抑制剂对大鼠胰十二指肠移植后缺血再灌注损伤的保护作用海南医学院学报,2009,15(10):1217-1220.
[38]Hargrave BY, Tiangco DA, Lattanzio FA, et al. Cocaine, not morphine, causes the generation of reactive oxygen species and activation of NF-kappaB in transiently cotransfected heart cells. Cardiovasc Toxicol, 2002, 3:141-151.
[39]王鄂友,胡刚,刘先义,等.参附注射液对缺血再灌注大鼠肠黏膜NF-κB和表达色影响.中国中医急症,2005,14(3):252-253.
[40]孟庆涛,夏中元,刘先义,等.参附对再灌注期间肠粘膜上皮细胞凋亡的抑制作用及机制探讨[J].临床麻醉学杂志,2004 ,20 (8) :498 - 500.
[41]宋卫兵,吕永慧,李亚南,等肠炎清通过抑制NF-κB活性对大鼠肠黏膜起抗炎作用.南方医科大学学报,2009,29(7):1431-1434.
[2]杨延芳,肠缺血再灌注肺损伤信号转导机制.现代医药卫生,2006,22(22):3445-3447.
[3]刘克玄,周军.丙泊酚对大鼠肠缺血再灌注所致肺损伤的保护机制[J].中华胃肠外科杂志,2004,7(4):326.
[4]盛志勇,胡森.多器官功能障碍综合征.北京科学出版社,1999:20-21.[5] BoyleEM, et al. AnnThorac Surg 1997, 63(1): 277-284.
[6] Li C, et al. Am J Physiol 1999; 276(2): H543-H552.
[7] Zou L, Atmwaybi B, Kone B C. et a1.Effects of NF-КB inhibition on mesenteric ischemia-reperfusion injury[J].Am J Physiol Gastr0intest Liver Physicl ,2003,284(4):G713-G721
[8] Tian XF. Yan JH, H YH, et a1. Effect of nuclear factor kappaB on intercellular adhesion molecule 1 expression and neutrophil infiltration in lung injury induced by intestinal ischemia/repeffusion in rats[J].World Gastroenterol, 2006, 12(3):388.
[9] Itai T, Tanaka M, Nagata S. Processing of tumor necrosis factor by the membrane bound T-NF-αlpha converting enzyme, but not its truncated soluble form [J]. Eur J Biochem, 2001, 26(8):2074-2082.
[10] CHO JE,KIM JE, et al. Epidural sufentanil provides better analgesia from 24h after surgery compared with epidural fentanyl in children [J]. Acta Anaesthesiolo Scand,2008, 52(10):1360-1363.
[11] Borgdorff PJ, Lonescuti, Houweling PL, et al. Large-dose intrathecal sufentanil prevents the hormonal stress response during major abdominal surger :a comparison with intravenous sufentanil in a prospective randomized trial[J].Anesth Analg ,2004,99(4):1114-1120.
[12]潘振祥,段立波,张春城.舒芬太尼术后PCEA对细胞因子、皮质醇的影响[J].临床麻醉学杂志,2006,22(11):856-857.
[13] Mallick IH, Yang W, Winslet MC, et al. Ischemia-reperfusion injury of the intestine and protective strategies against injury.Dig Dis Sci.2004;49(9):1359-77.
[14] Yao JH, Zhang XS, Zheng 55, et al. ProPhylaxis with earnosol attenuates liver injury indueed by intestinal isehemia/rePerfusion. World J Gastroenterol.2009; 15(26):3240-3245.
[15] Wu XT, Li JS, Zhao XF, Zhuang W, Feng XL. Modified techniques of hetero-topictotal small intestinal transplantation in rats.World J Gastroente-rol.2002, 8:758-762.
[16] Stallion A, Kou TD, Latifi SQ, et al. Ischemia/reperfusion: a clinically relevant mode of intestinal injury yielding systemic inflammation. J Pediatr Surg.2005, 40(3):470-477.
[17] Hassoun HT, Kone BC, Mercer DW, et al. Post-injury multiple organ failure: the role of the gut. Shock, 2002:15(1):1-10.
[18] Pierro A and Eaton S. Intestinal ischemia reperfusion injury and multisystem organ failure. Semin Pediatr Surg. 2004; 13(1):11-17.
[19] Ware LB, Matthay MA. The acute respiratory distress syndrome .N Engl J Med. 2000; 342(18):1334-1349.
[20] Prakanrattana U, Suksompong S, .ComParision of sufentanil and fentanyl for surgieal repair of congenitalcardiac defects. J Med Assoc Thai, 2002,85(3):807-14.
[21]金昔陆.池志强.阿片受体激动剂舒芬太尼的药理作用和应用.中国现代应用药学杂志,1999,16(1):1-5.
[22] Monk JP, Beresford R, Ward A. Sufentail A Review of its Pharmacological Properties and Therapeutic Use. ADIS Drug Information Services, 1988, Drugs 36:286-313.
[23]黄继汉,黄晓晖,陈志扬.药理试验中动物间和动物与人体间的等效剂量换算.中国临床药理学与治疗学,2004,9(9):1069-72.
[24]张成明,于金玲,张岩.舒芬太尼对家兔急性肺损伤的影响.中国危重病急救医学,2008,20(2):108-110.
[25]刘鲲鹏,孙海涛,薛富善,等.不同剂量的舒芬太尼预处理对大鼠的延迟性心肌保护作用,中华麻醉学杂志,2009,(5);405-408.
[26]张冬梅,常亚恬,徐向辉,等.舒芬太尼预先给药对大鼠心肌缺血再灌注损伤的影响.中华麻醉学杂志, 2008,28(10):932-935.
[27]张冬梅,侯春丽,常亚恬,等.舒芬太尼预处理对缺血再灌注大鼠心肌梗死范围及心肌酶的影响.实用医学杂志,2009,25(15):2430-2433.
[28]李进,袁世荧,丰新民,等.舒芬太尼延迟后处理对兔心肌缺血再灌注损伤的影响,中华麻醉学杂志, 2009, 29(8):692-695.
[29]金利达,林丽娜,王俊等.舒芬太尼预先给药对兔心肌缺血再灌注的影响.中华麻醉学杂志,2008,28(9):855-857.
[30] Zhao ZQ, Corvera JS, Halkos ME, et al.Inhibition of myocardial injury by ischemic post-conditioning during reperfusion: comparison with ischemic pre-conditioning [J] . Am J Physiol Heart Circ Physiol. 2003, 285(2):H 579-H 588.
[31]姚树桐,刘秀华,赵秀梅等.钙调神经磷酸酶的抑制参与大鼠心脏缺血后处理的保护作用[J].中国病理生理杂志,2008,24(12):2289-2294.
[32]姚树桐,刘秀华,汤旭明等.缺血后处理改善脑缺血再灌注大鼠软脑膜微循环[J].中国病理生理杂志,2009,25(3):451-455.
[33]姚树桐,赵秀梅,刘秀华.细胞间黏附分子-1抑制参与大鼠小肠缺血后处理的保护作用[J].中国微循环,2008,12(2):69-72.
[34]毛张凡,杜心灵,孙宗全,夏家红,阿片受体参与大鼠缺血后处理的心肌保护作用,华中科技大学学报(医学版),2007,36(5):601-613.
[35] Venkatapuram S ,Wang C ,Krolikowski JG ,et al .Inhibition of apoptotic protein P53 lowers the threshold of isoflurane induced cardio protection during early reperfusion in rabbits [J].Anesth Analg ,2006,103(6):1400-1405.
[36] Obal D,Rascher K, Favoccia C,et al. Post-conditioning by a short administration of desflurane reduce renal reperfusion injury after differing of ischaenia tines in rats .British J Anaesth,2006,97:783-791.
[37] Chen H, Xing B,Liu X et al .Ischemic postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat[J]. TransplInt , 2007,17(2):71.
[38]姚树桐,李玉珍,刘秀华,等.缺血后处理对小肠缺血-再灌注损伤大鼠肠系膜微循环的影响[J].微循环杂志,2007,17(2):1.
[39]林世清,黄文起,冯霞,等.缺血后处理对兔小肠缺血再灌注损伤的影响.中华麻醉学杂志,2007,27(11): 1042 -1044.
[40]郝志强,王为忠,李孟彬,等.丙酮酸对大鼠小肠缺血再灌注的保护作用[J].中国临床康复,2004,8(2): 276-277.
[41]文斌,屠伟峰,何静等.大鼠全肠道缺血再灌注后肠道组织和肠道外器官损伤的研究实用医学杂志,2003, 19(2):126-128.
[42] Churg A, Dai J, Tai H, et al. Tumor necrosis factor-alpha is central to acute cigarette smo-ke induced inflammation and connective tissue breakdown[J]. Am J Respir Crit Care Med, 2002,16(6):849-854.
[43] Aldonyte R, Jansson L, Piitulainen E, et al. Circulating monocytes from healthy individuals and COPD patients [J]. Respir Res, 2003,4(2):11.
[44]曲敬祥.慢性阻塞性肺疾病患者血清IL-8和TNF-α测定的临床意义[J].山东医药,2007,47(22): 80.
[45] Souza AL , Jr ,Pontes B ,et al .Gut isocheimal/reperfusion activates lung macrphages for tumor necrosis factor and hydrogen peroxide production .J Trauma 2000;49(2);232-2365
[46] Yao YM, Bahrami S,Redl H ,et al.IL-6 release after intestinal ischemia/reperfusion in rats B, et al. Intestinal ischemia/reperfusion induces bronchial hyper reactivity and increases serum TNF-αin rats . Clinics 2006; 61(1);21-28.
[47]张树平,胡涛,栾海云,李庆忠,李淑翠,刘金平;肠缺血再灌注大鼠肺及血液白细胞介素6、白细胞介素8和肿瘤坏死因子变化与辅酶Q的干预,中国组织工程研究与临床康复;2007,11(27),5429-5431.
[48]姚咏明,田惠明,王亚军等.肿瘤坏死因子在肠缺血所致多器官损伤中的作用.中华整形烧伤外科杂志,1994,10;282-284.
[49] Albert S, Baldwin Jr. The NF-κB and IκB proteins: New discoveries and Insights. Annu Rev Immunol, 1996,14:649-681.
[50] Muller JM, Ziegler-Heitbrock HW, Baeuerle PA. Nuclear factor kappa B, amediator of lipopolysaccharide effects. Immunobiol, 1993, 187:233-256.
[51] Woronicz JD, Gao X, Cao Z, et al. IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK.Science, 1997,278:866-869.
[52] Chandrasekar B, Streitmen JE, Colston JT ,et al.Inhibition of nuclear factor kappaB attenuats proinflammatory cytokine and inducible nitric-oxide synthase expressiom in postischemic myocardium.Biochim Biophys Acta, 1998,1406:91-106.
[53] Blackwell TS, Christman JW. The role of nuclear factor-kappa-B in cytokinegene regulation. Am J Resir Cell Mol Biol, 1997,17:3-9.
[54] Bevilacqua MP, Pober JS, Mendrick DL, et al. Identification of an inducible endothelial-leukocyte adhesion molecule. Proc Natl Acad Sci U S A, 1987, 84:9238-9242.
[55] Zwacka RM, Zhang Y, Zhou W, et al.Ischemia/reperfusion injury in the liver of BALB/c miceactivates AP-1and nuclear factor-κB independently of IκB degradation.Hepatology,1998,28:1022-1030.
[1] Edelman DA, Sugawa C, Lower gadtrointestinal bleeding, a review [J]. Surg Endose,2007 ,21(4):514.
[2]杨延芳,肠缺血再灌注肺损伤信号转导机制;现代医药卫生,2006,22(22):3445-3447
[3]刘克玄,周军.丙泊酚对大鼠肠缺血再灌注所致肺损伤的保护机制[J].中华胃肠外科杂志,2004,7(4);326
[4]盛志勇,胡森,多器官功能障碍综合征.北京科学出版社,1999.20-21.
[5] Boyle EM, et al. Ann Thorac Surg 1997; 63(1): 277-284.
[6] Li C, et al. Am J Physiol 1999; 276(2): H543-H552.
[7] Sen R, Baltimore D. Multiple nuclear factors interact with the immunoglobulim enhancer sequences. Cell, 1986,46:705-716.
[8] Albert S, Baldwin Jr. The NF-κB and IκB proteins: New discoveries and Insights. Annu Rev Immunol, 1996,14:649-681.
[9] Muller JM, Ziegler-Heitbrock HW, Baeuerle PA. Nuclear factor kappa B, amediator of lipopolysaccharide effects. Immunobiol, 1993,187:233-256.
[10] Woronicz JD, Gao X ,Cao Z, et al. IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK.Science, 1997,278:866-869.
[11] Chandrasekar B, Streitmen JE, Colston JT ,et al.Inhibition of nuclear factor kappaB attenuats proinflammatory cytokine and inducible nitric-oxide synthase expressiom in postischemic myocardium.Biochim Biophys Acta, 1998,1406:91-106.
[12] Blackwell TS, Christman JW. The role of nuclear factor-kappa-B in cytokinegene regulation. Am J Resir Cell Mol Biol, 1997, 17:3-9.
[13] Bevilacqua MP, Pober JS, Mendrick DL, et al. Identification of an inducible endothelial-leukocyte adhesion molecule. Proc Natl Acad Sci U S A,1987,84:9238-9242.
[14] Zwacka RM, Zhang Y, Zhou W, et al.Ischemia/reperfusion injury in the liver of BALB/c miceactivates AP-1 and nuclear factor-κB independently of IκB degradation.Hepatology,1998,28:1022-1030.
[15] Akira S,Hirano T,Taga T,et al.Biology of multifunctional cytokines:IL-6 related molecules(IL-1 and TNF-α).FASEB J,1990,4:2860-2867.NF-κB.
[16]Arenzana Seidedos F ,Turpin P ,Rodriguez M ,et al. Nuclear localization of IκB promotes active transport of NF -κB from the nucleus to the cytoplasm[J]. J Cell Sci , 1997 ,110 (3) :369 - 378.
[17] Schmidt K N ,Traenckner EB M , Meier B ,et al. Induction of oxidative stress by odadaic acid is required for activation of transcription factor NF–κB[J]. J Biol Chem , 1995 ,270 (45) :27136 - 27142.
[18] Zou L, Attuwaybi B, Kone BC.Effects of NF-Kappa B inhibition on mesenteric ischemia-reperfusion injury [J].Am Physiol ,2003,284(4):G713.
[19] Arenzana-seisdedos F,Turpin P, Rodriguez M,et al.Nuclear localizaion of IkB promotes active transport of NF-KB from the nucleus to the cytoplasm[J].Cell Sei,1997,110(pt3):369.
[20]Yeh KY, et al.Gastroenterology 2000; 118(3): 525-534.
[21]Hassoun H T , Kozar R A , Kone B C ,et al. Intraischemic hypothermia differentially modulates oxidative stress proteins during mesenteric ischemia/ reperfusion[J]. Surgery,2002 ,32 (2) :369 - 376.
[22]Zou L ,Attuwaybi B , Kone BC. Effects of NF - kappaB inhibition on mesenteric ischemia/ reperfusion injury [J] . Am J Physiol ,2003 ,284 (4) : G713-721.
[23]邬善敏,张训臣.肠上皮细胞凋亡与肠缺血损伤及再生修复的试验研究[J].中华急诊医学杂志,2003 ,12 (9) :604- 606.
[24]Ikeda H ,Suzuki Y,Suzuki M ,et al. Apoptosis is a major mode of cell death caused by ischemia and ischemia/ reperfusion injury to the rat intestinal epithelium. Gut ,1998 ,42 :530 - 537.
[25] Noda T, et al. Am J Physiol 1998; 274(2 Pt1): G270-G276.
[26]Gupta RA, et al. J Biol Chem 2001; 276(33): 31059-31066.
[27]李晓鲁,袁志强,彭毅志.重组腺病毒介导的HSP70转染对肠上皮细胞缺氧再复氧损伤的保护作用.中华医学杂志.2002,82(16)1102-1104.
[28] Feinstein DL, et al. J Biol Chem 1996; 271(30): 17224-17232.
[29] Boyle EM, et al. Ann Thorac Surg 1999; 68(5): 1949-1953.
[30]史晓峰,刘敦贵. 1 ,6 -二磷酸果糖在大鼠小肠缺血再灌注损伤中的保护作用[J].中国临床营养杂志, 2003 ,11 (4) :278 - 280.
[31]方天翎,唐朝晖,胡元龙,夏穗生,等.谷氨酰胺对缺血再灌注损伤早期小肠粘膜细胞凋亡的影响[J].中国临床营养杂志,2003 ,11 (1) :40 - 43.
[32]谢伟霖,蒋更如,尤新民等.N-乙酰半胱氨酸对多器官功能障碍综合征大鼠器官的保护作用及其机制上海医学,2009,32(11):987-991.
[33]Anrather J, et al.J Clin Invest 1997; 99(4): 763-772.
[34].Gan H, Ouyang Q, Chen Y , Liang F . The effects of nuclear factor-kappa B p65 antisenseoligonucleotides on expression of proinfl amatory cytokines in lamina propria mononuclear cells from patients with ulcerative colitis. Shengwu Yixue Gongchengxue Zazhi 2003; 20: 268-272
[35]李弼民,吕农华,谢勇等.NF-KB P65反义寡核苷酸对TNBS结肠炎小鼠肠黏膜细胞因子和NF-KB表达的影响.世界华人消化杂志,2008;16(17):1926-1931.
[36]李英华,田晓峰,王真真.NF-KB对肠缺血再灌注肝损伤P-选择素表达和中性粒细胞浸润的作用世界华人消化杂志2006,14(5):486-490.
[37]陈茂松,崔海宁,张克君,等.核因子-κB抑制剂对大鼠胰十二指肠移植后缺血再灌注损伤的保护作用海南医学院学报,2009,15(10):1217-1220.
[38]Hargrave BY, Tiangco DA, Lattanzio FA, et al. Cocaine, not morphine, causes the generation of reactive oxygen species and activation of NF-kappaB in transiently cotransfected heart cells. Cardiovasc Toxicol, 2002, 3:141-151.
[39]王鄂友,胡刚,刘先义,等.参附注射液对缺血再灌注大鼠肠黏膜NF-κB和表达色影响.中国中医急症,2005,14(3):252-253.
[40]孟庆涛,夏中元,刘先义,等.参附对再灌注期间肠粘膜上皮细胞凋亡的抑制作用及机制探讨[J].临床麻醉学杂志,2004 ,20 (8) :498 - 500.
[41]宋卫兵,吕永慧,李亚南,等肠炎清通过抑制NF-κB活性对大鼠肠黏膜起抗炎作用.南方医科大学学报,2009,29(7):1431-1434.