异丙酚对大鼠小肠缺血与再灌注损伤的保护作用
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摘要
目的建立大鼠小肠缺血与再灌注模型,通过观察肠脂肪酸结合蛋白和丙二醛含量变化,结合小肠组织病理学改变,探讨异丙酚处理对大鼠小肠缺血与再灌注损伤的影响,为临床研究提供实验参数和依据。
方法成年健康SD雄性大鼠30只,体重250～300g。随机分为对照组(C组)、小肠缺血与再灌注组(I/R组)和异丙酚处理组(R组),每组l0只。通过夹闭肠系膜上动脉(SMA)制作小肠缺血与再灌注损伤模型。对照组仅在无菌条件下打开腹腔,不夹闭SMA;I/R组沿腹中线打开腹腔,游离肠系膜上动脉根部,用无损伤动脉夹夹闭SMA 60min,然后松开动脉夹行再灌注60min;R组在夹闭SMA前10min给予异丙酚10mg/kg静脉注射,随后按10mg/(kg·h)维持处理。各组分别于缺血前、缺血后15、30、60 min和去除无损伤动脉夹再灌注后30、60 min采集静脉血用于检测肠脂肪酸结合蛋白(I-FABP)。最后取空肠组织5cm,用于检测丙二醛(MDA)含量及常规制备全层石蜡切片行HE染色,光镜下观察小肠组织病理学变化。
结果C组肠脂肪酸结合蛋白(I-FABP)水平在整个实验过程中变化不明显,保持在较低水平;I/R组和R组I-FABP水平在缺血15 min后可迅速达到缺血前数十倍,缺血30 min后可达到高峰,再灌注30 min后下降,但再灌注60min后仍为缺血前的数十倍;R组I-FABP水平与I/R组比较在缺血及再灌注期间内明显降低,两组比较存在着显著差异(P<0.01)。与C组相比,I/R和R组小肠组织MDA含量均明显升高(P<0.01);与I/R组相比,R组小肠组织MDA含量降低,两组比较差异具有显著性(P<0.05)。小肠组织病理学结果:C组小肠未见明显组织学异常改变;I/R组可见小肠粘膜层上皮和大部分腺体坏死,粘膜固有层血管扩张充血,组织水肿,其间有较多的炎症细胞浸润。R组小肠损伤程度较I/R组明显减轻。
结论1、静脉异丙酚处理可以降低大鼠小肠缺血与再灌注损伤后血清I-FABP水平和小肠组织MDA含量,明显减轻光镜下小肠组织病理学损伤程度。2、静脉异丙酚处理对大鼠小肠缺血与再灌注损伤有较好的保护作用。3、异丙酚处理对大鼠小肠缺血与再灌注损伤的保护机制可能与改善小肠粘膜血液循环病理生理学机制及抑制缺血与再灌注氧自由基的生成有关。
Objective To set up a rat model of intestinal ischemia and reperfusion(I/R).To evaluate the changes of intestinal fatty acid binding protein (I-FABP),and Malondialdehyde(MDA),and the morphological changes of intestinal mucosa To investigate the effect of propofol on gut injury following intestinal ischemia and reperfusion,and to provide the basic experimental parameters and evidences.
Methods Thirty major adult male Sprague-Dawley(SD) rats (weighting250～300g) were randomly divided into 3(n=10 each):control group(C); Ischemia and Reperfusion group (I/R);propofol group(R).A rat model of intestinal ischemia and perfusion was stablished by blocking the superior mesenteric artery(SMA) with clap for 60 min followed by 60 min reperfusion. Group C rats underwent only midline laparotomy without blocking superior mesemteric artery.Group I/R and R rats underwent a midline laparotomy and then SMA isolation (with a microvascular clip).The SMA occlusion lasted for 60 minutes followed by 60 minutes of reperfusion.Group R rats underwent a additional administration of propofol(10mg/kg) 10min before ischemia and followed by continuous infusion at 10mg/(kg·h). Blood samples were collected from the inferior vena cava prior to ligation、15、30、60 minutes after ligation and 30、60 minutes after reperfusion for determination of I-FABP.The animals were all killed at the end of 1h reperfusion and a small segment of ileum was taken for determination of MDA.The ileum slices were made and pathological changes were also observed under microscope in each group.
Results In group C,the level of I-FABP had no significant difference and keep at a low level during the operation time.In group I/R and group R the level of I-FABP increased 15 minutes after ligation and peaked at 30 minutes.It dropped after 30 minutes of reperfusion.But at 60 minutes after I/R injury,it was number of times of the nomlal serum level of I-FABP.Compare with group I/R,the I-FABP in group R decreased during the period of ligation and reperfusion and there was significant difference between the Group I/R and R (P<0.01).The MDA concentrations in group I/R and group R were significantly higher than those in group C (P<0.01) during the period of ligation and reperfusion.The MDA concentrations in group R were lower than those in group I/R (P<0.05).The morphological changes of intestinal tissues were observed with light microscopy.With the staining of HE, In group C,it cannot be seen abnormality in small intestinal tissue.In group I/R the morphological changes of intestinal mucosa could be observed.The mucous layer appeared necrotic,some intestinal mucosal cells shed to enteric cavity,and submucous layer had hyperemia and edema obviously.In group R the necrosis of intestinal mucosa was ameliorated and damage was not obvious as compared with the group I/R.
Conclusion Administration with propofo1 can reduce the level of I-FABPand MDA and attenuate the injury of intestinal mucosa in rats after intestinal ischemia and reperfusion injury.Administration with propofo1 can provide significant protection against intestinal ischemia and reperfusion injury,which may be attributed to the ameliorative blood circulation effect and antioxidant effect of propofo1.
方法成年健康SD雄性大鼠30只,体重250～300g。随机分为对照组(C组)、小肠缺血与再灌注组(I/R组)和异丙酚处理组(R组),每组l0只。通过夹闭肠系膜上动脉(SMA)制作小肠缺血与再灌注损伤模型。对照组仅在无菌条件下打开腹腔,不夹闭SMA;I/R组沿腹中线打开腹腔,游离肠系膜上动脉根部,用无损伤动脉夹夹闭SMA 60min,然后松开动脉夹行再灌注60min;R组在夹闭SMA前10min给予异丙酚10mg/kg静脉注射,随后按10mg/(kg·h)维持处理。各组分别于缺血前、缺血后15、30、60 min和去除无损伤动脉夹再灌注后30、60 min采集静脉血用于检测肠脂肪酸结合蛋白(I-FABP)。最后取空肠组织5cm,用于检测丙二醛(MDA)含量及常规制备全层石蜡切片行HE染色,光镜下观察小肠组织病理学变化。
结果C组肠脂肪酸结合蛋白(I-FABP)水平在整个实验过程中变化不明显,保持在较低水平;I/R组和R组I-FABP水平在缺血15 min后可迅速达到缺血前数十倍,缺血30 min后可达到高峰,再灌注30 min后下降,但再灌注60min后仍为缺血前的数十倍;R组I-FABP水平与I/R组比较在缺血及再灌注期间内明显降低,两组比较存在着显著差异(P<0.01)。与C组相比,I/R和R组小肠组织MDA含量均明显升高(P<0.01);与I/R组相比,R组小肠组织MDA含量降低,两组比较差异具有显著性(P<0.05)。小肠组织病理学结果:C组小肠未见明显组织学异常改变;I/R组可见小肠粘膜层上皮和大部分腺体坏死,粘膜固有层血管扩张充血,组织水肿,其间有较多的炎症细胞浸润。R组小肠损伤程度较I/R组明显减轻。
结论1、静脉异丙酚处理可以降低大鼠小肠缺血与再灌注损伤后血清I-FABP水平和小肠组织MDA含量,明显减轻光镜下小肠组织病理学损伤程度。2、静脉异丙酚处理对大鼠小肠缺血与再灌注损伤有较好的保护作用。3、异丙酚处理对大鼠小肠缺血与再灌注损伤的保护机制可能与改善小肠粘膜血液循环病理生理学机制及抑制缺血与再灌注氧自由基的生成有关。
Objective To set up a rat model of intestinal ischemia and reperfusion(I/R).To evaluate the changes of intestinal fatty acid binding protein (I-FABP),and Malondialdehyde(MDA),and the morphological changes of intestinal mucosa To investigate the effect of propofol on gut injury following intestinal ischemia and reperfusion,and to provide the basic experimental parameters and evidences.
Methods Thirty major adult male Sprague-Dawley(SD) rats (weighting250～300g) were randomly divided into 3(n=10 each):control group(C); Ischemia and Reperfusion group (I/R);propofol group(R).A rat model of intestinal ischemia and perfusion was stablished by blocking the superior mesenteric artery(SMA) with clap for 60 min followed by 60 min reperfusion. Group C rats underwent only midline laparotomy without blocking superior mesemteric artery.Group I/R and R rats underwent a midline laparotomy and then SMA isolation (with a microvascular clip).The SMA occlusion lasted for 60 minutes followed by 60 minutes of reperfusion.Group R rats underwent a additional administration of propofol(10mg/kg) 10min before ischemia and followed by continuous infusion at 10mg/(kg·h). Blood samples were collected from the inferior vena cava prior to ligation、15、30、60 minutes after ligation and 30、60 minutes after reperfusion for determination of I-FABP.The animals were all killed at the end of 1h reperfusion and a small segment of ileum was taken for determination of MDA.The ileum slices were made and pathological changes were also observed under microscope in each group.
Results In group C,the level of I-FABP had no significant difference and keep at a low level during the operation time.In group I/R and group R the level of I-FABP increased 15 minutes after ligation and peaked at 30 minutes.It dropped after 30 minutes of reperfusion.But at 60 minutes after I/R injury,it was number of times of the nomlal serum level of I-FABP.Compare with group I/R,the I-FABP in group R decreased during the period of ligation and reperfusion and there was significant difference between the Group I/R and R (P<0.01).The MDA concentrations in group I/R and group R were significantly higher than those in group C (P<0.01) during the period of ligation and reperfusion.The MDA concentrations in group R were lower than those in group I/R (P<0.05).The morphological changes of intestinal tissues were observed with light microscopy.With the staining of HE, In group C,it cannot be seen abnormality in small intestinal tissue.In group I/R the morphological changes of intestinal mucosa could be observed.The mucous layer appeared necrotic,some intestinal mucosal cells shed to enteric cavity,and submucous layer had hyperemia and edema obviously.In group R the necrosis of intestinal mucosa was ameliorated and damage was not obvious as compared with the group I/R.
Conclusion Administration with propofo1 can reduce the level of I-FABPand MDA and attenuate the injury of intestinal mucosa in rats after intestinal ischemia and reperfusion injury.Administration with propofo1 can provide significant protection against intestinal ischemia and reperfusion injury,which may be attributed to the ameliorative blood circulation effect and antioxidant effect of propofo1.
引文
[1] Goteri G,Lucarini G,Pieramici T,et al. Endothelial cell Survivin is involved in the growth of ovarian endometriotic cyst[J].Anticancer Res,2005,(6B): 4313- 4318.
[2] Mole DJ,Taylor MA,McFerran NV,Diamond T.The isolated perfused liver response to a’second hit’of Portal endotoxin during severe acute pancreatitis.Pancreatology, 2005,5:475-485.
[3] Shimizu K,Oguar H,Goto M,Asahara T,Nomoto K,Morotom i M,Yoshiya K,Matsushima A,Sumi Kuwagata Tanaka H,Shimazu L Sugimoto H. A1tered gut flora and environment in patients with severe SIRS.J Trauma 2006,60:126-133.
[4] Beuk RJ, Oude Egbrink MG, Kurvers HA, et al.schemia/reperfusion injury in rat mesenteric venules: red blood cell velocity and leukocyte rolling.J Pediatr Surg, 1996,31:512-515.
[5] Gonzalez AP,Sepulveda S,Massberg S,et al.In vivo fluorescence microscopy for the assessment of microvascular reperfusion injury small bowel transplants in rats.Transplantation,1994,58:403-408.
[6] Marks WH,Gollin G.Biochemical detection of small intestinal allograft rejection by elevated circulating levels of serum intestinal fatty acid binding protein.Surgery,1993,114(2):206-210.
[7] Go llin G,Marks WH.Elevation of circulating intestinal fattv acid binding protein in a luminal contents-initiated model of NEC.J Pediatr Surg,1993,28(3):367-371.
[8] AM Koivusalo, I Kellokumpu, S Ristkari and L Lindgren. Splanchnic and renal deterioration during and after laparoscopic cholecystectomy: a comparison of the carbon dioxide pneumoperitoneum and the abdominal wall lift method. Anesthesia & Analgesia, 2004,Vol 85, 886-891.
[9] Niewold TA,Meinen M,van der Meulen J.Plasma intestinal fatty acid binding protein(I-FABP)concentrations increase following intestinal ischemia in pigs.Res Vet Sei,2004,77(1):89-91.
[10] Sharma MK,Denovan-Wright EM,Degrave A,et a1.Sequence,linkage mapping and early developmental expression of the intestinal-type fatty acid binding protein gene(fabp2)from zebrafish(Danio rerio).Comp Biochem Physiol B Biochem Mol Biol,2004,138(4):391-398.
[11]张硕森,李宏杰,崔和勤,等.家兔肠缺血再灌注损伤时脂质过氧化的变化及其意义.天津医科大学学报,1998,4:325-328.
[12] Yassin MM,Barros D’Sa AA,Parks TG,McCaigue MD,Leggett P,Halliday MI,Rowlands BJ.Lower limb ischaemia-reperfusion injury alters gastrointestinal structure and function.Br J Surg 1997;84:1425-1429.
[13] Chiu CJ,Mcardle AH,et a1.Intestinal mucoslesion in low flow states.A morphologic hemodynamic and metabolic reappraisa1.Arch Surg,1970,101:478-483.
[14] Takala I.Determinants of splanchnic blood flow.Br J Anaesth 1996,77:50-58
[15] Hinnebusch BF,Ma Q,Henderson J W,et a1.Enterocyte response to ischemia is dependent on differentiation state.J Gastrointest Surg,2002,6(3):403-409
[16]刘海光,杜丹,伦明辉,等.缺血再灌注损伤降低肠粘膜屏障功能的初步研究[J].大连医科大学学报,2004,246(1):l7-19.
[17] Calvet X,Baigorri F,Duarte M, et a1.Effect of sucralfateon gastric intramucosal PH in critically ill patients.Intensive Care Med,1997,23:738-742
[18]华鲁纯,孟淑美,杨俭,等.小肠缺血再灌注损伤时自由基清除剂及MDA变化的实验研究.中国微循环,1999,11(3):205-207.
[19] RuizGines JA,LopezOngil S,GonzalezRubio M,et a1.Reative oxygen species induce proliferation of bovine aortic endothelial cells[J].J Cardiovasc Pharmacol,2000,35(1):109-113.
[20]毛新俊,胡振快,文俊,等.异丙酚对兔小肠缺血再灌注损伤的保护作用.中华麻醉学,2005,9:704-705.
[21] Pelsers MM, Hemtens WT, Glatz JF. Fatty acid binding proteins as plasma markm of itssue injury. Clinic him Acta, 2005, 352(1 -2):15-35.
[22]沈涤华,施诚仁,吴燕,等.肠脂肪酸结合蛋白在肠缺血早期诊断的意义中华麻醉学,2004,25(2):176-178.
[23]刘牧林,张嘉,刘瑞林,等.肠脂肪酸结合蛋白和D-乳酸早期诊断肠缺血-再灌注损害的实验研究.中华创作杂志,2006,22(10):767-770.
[24] Nakatani T,Saito Y,Sakura S et a1.Haemodynamic effects of thoracic epidural anaesthesia during induction of anaesthesia:an investigation into the effects of tracheal intubatien during target-controlled infusion of propofo1.Anaesthesia,2005,60(1):530-536.
[25] Kolkman J,Steverink PJ,Groeneveld AB,et a1.Characteristics of time dependent PCO2 tonomotry in the normal human stomach.Br J naesth,l998,81:669-675.
[26] Cheng YJ,Wang YP,Chien CT,et a1.Small-dose pmpofol sedation attenuates the formation of reactive oxygen species in tourniquet-induced isehemia-repeffusion injury under spinal anesthesia[J].Anesth A nalg,2002,94(6):16-22.
[27] Murphy PG.Myers DS,Davies MJ,et a1.The antioxidant potential of propofol(2,6-dissopropylpheno1).Br J Aanesth,1992,68:613-618.
[28]王亚平,常业恬,钟林.异丙酚对过氧化氢所致的血管内皮细胞损伤的保护作用.中华麻醉学杂志,1998,l8:165-168.
[29] Taniguchi T,kanakura H,kamamoto k,Y effects of posttreatment with propofol on mortality and cytokine responses to endotoxin-induced shock in rats.Crit Care Med ,2002,30:904-907.
[1] Goteri G,Lucarini G,Pieramici T,et al.Endothelial cell Survivin is involved in the growth of ovarian endometriotic cyst[J].Anticancer Res,2005,(6B):4313-4318.
[2] Yang-Z J,Bosco G,Montante A,et a1.Hyperbaric 02 reduce intestinal ischemia reperfusion induced TNF-alpha production and lung neutrophic sequestration[J].Eur J Appl Physic1.2001,85(12):96.
[3] De Souza DA,Greene LJ.Intestinal permeability and systemic infections in critically ill patients.Effect lf glutamine[J].crit Care MED,2005,33(5):1125-113 5.
[4] RuizGines JA,LopezOngil S,GonzalezRubio M,et a1.Reative oxygen species induce proliferation of bovine aortic endothelial cells[J].J Cardiovasc Pharmacol,2000,35(1):109-113.
[5] Castedo E,Segovia J,Escudero C,et al.Ischemia-reperfusion injury during experimental heart transplantation:evaluation of trimetazidineps cytoprotective effect[J].Rev Esp Cordial,2005,58(8):941-950.
[6]王长友,等.复方丹参对肠缺血再灌注损伤防治作用的实验研究[J].中华实用中西医杂志,2005,18(16):677-679.
[7]刘金保,冉丕鑫.粘附分子在缺血再灌注损伤中的作用[J].国外医学生理、病理科学与临床分册,1997,17(3):247.
[8]吕艺,盛志勇,黎君友,等肠缺血再灌注大鼠小肠血管内皮细胞ICAM-1表达的变化及其与肠损伤的关系[J].中华普通外科杂志.2000,15(3):145.
[9] Gross GJ,Kersten JR,Warltier DC.Mechanisms of postischemic contractile dysfunction[J].Ann Thorac Surg,1999,68(5):1898-1904.
[10]张润峰,李霞.丹参改善缺血再灌注血液流变学异常的作用机制研究[J].华西医学,2004,19(2):341-342.
[11] Ikeda H,suzuki Y,Suzuki M,et a1.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.
[12]徐斌,李琳,等活血清下法在小肠缺血再灌注时对细胞凋亡因子Apaf-1和Bcl-2的调控作用[J].天津医学,2007,35(8):598-599.
[13] W u B,Ootani A,Iwakiri R,Fujise T,Tsunada S,Toda S,Fujimoto K.Ischemic preconditioning attenuates ischemia-reperfusion-Induced mucosal apoptosis by inhibiting the mitochondria-dependent pathway in rat small intestine.AmJ Physiol Gastrointest Liver Physiol 2004;286:G580-587.
[14]林世清,黄文起,等.缺血后处理对兔小肠缺血再灌注损伤的影响[J].中华麻醉学,2007,27(11):1042-1044.
[15] Gateau-Roesch O,Argaud L,Ovize M.Mitochondrial permeability transition pore and postconditioning [J].Cardiovasc Res,2006,70(2):264-273.
[16] Argaud L,Gateau-Roesch O,Raisky O,et al.Postconditioning inhibits mitochondrial permeability transition [J].Circulation,2005,111(2):194-197.
[17]褚薇薇,武步强,等.缺血后处理对大鼠肠缺血再灌注损伤肠粘膜细胞线粒体的影响[J].西安交通大学学报,2008,29(14):409-411.
[18] Sola A,Alfaro V,Pesguero J, et al.Co2 in static mesenteric venous blood during intestinal ischemia and ischemic priconditioning in rast [J].shock,2001,16(5):403-408.
[19] Kojima M,Iwakiri R,wu B,et a1.Effects of antioxidative agents on apoptosis induced by ischaemia-reperfusion in rat intestinal mucosa[J].Aliment Pharmacol Ther,2003,18(Suppl 1):139-145.
[20] Sun Z,Olanders K,Lasson A,et a1.Effective treatment of gut barrier dysfunction using an antioxidant,a PAF inhibitor,and monoelonal antibodies against the adhesion molecule PECAM-1 [J].J Surg Res,2002,105(2):220-233.
[21] Ilhan H,Alatas O,Tokar B,et a1.Effects of the anti-ICAM-1 monoclonal antibody,allopurinol,and methylehe blue on intestinal reperfusion injury[J].J Pediatr Surg,2003,38(11):1591-1595.
[22]张华,陈聪德,等.红花对兔肠缺血再灌注损伤后肠壁ICAM-1表达的影响[J].中国中医医结合外科,2009,15(2) :170-173.
[2] Mole DJ,Taylor MA,McFerran NV,Diamond T.The isolated perfused liver response to a’second hit’of Portal endotoxin during severe acute pancreatitis.Pancreatology, 2005,5:475-485.
[3] Shimizu K,Oguar H,Goto M,Asahara T,Nomoto K,Morotom i M,Yoshiya K,Matsushima A,Sumi Kuwagata Tanaka H,Shimazu L Sugimoto H. A1tered gut flora and environment in patients with severe SIRS.J Trauma 2006,60:126-133.
[4] Beuk RJ, Oude Egbrink MG, Kurvers HA, et al.schemia/reperfusion injury in rat mesenteric venules: red blood cell velocity and leukocyte rolling.J Pediatr Surg, 1996,31:512-515.
[5] Gonzalez AP,Sepulveda S,Massberg S,et al.In vivo fluorescence microscopy for the assessment of microvascular reperfusion injury small bowel transplants in rats.Transplantation,1994,58:403-408.
[6] Marks WH,Gollin G.Biochemical detection of small intestinal allograft rejection by elevated circulating levels of serum intestinal fatty acid binding protein.Surgery,1993,114(2):206-210.
[7] Go llin G,Marks WH.Elevation of circulating intestinal fattv acid binding protein in a luminal contents-initiated model of NEC.J Pediatr Surg,1993,28(3):367-371.
[8] AM Koivusalo, I Kellokumpu, S Ristkari and L Lindgren. Splanchnic and renal deterioration during and after laparoscopic cholecystectomy: a comparison of the carbon dioxide pneumoperitoneum and the abdominal wall lift method. Anesthesia & Analgesia, 2004,Vol 85, 886-891.
[9] Niewold TA,Meinen M,van der Meulen J.Plasma intestinal fatty acid binding protein(I-FABP)concentrations increase following intestinal ischemia in pigs.Res Vet Sei,2004,77(1):89-91.
[10] Sharma MK,Denovan-Wright EM,Degrave A,et a1.Sequence,linkage mapping and early developmental expression of the intestinal-type fatty acid binding protein gene(fabp2)from zebrafish(Danio rerio).Comp Biochem Physiol B Biochem Mol Biol,2004,138(4):391-398.
[11]张硕森,李宏杰,崔和勤,等.家兔肠缺血再灌注损伤时脂质过氧化的变化及其意义.天津医科大学学报,1998,4:325-328.
[12] Yassin MM,Barros D’Sa AA,Parks TG,McCaigue MD,Leggett P,Halliday MI,Rowlands BJ.Lower limb ischaemia-reperfusion injury alters gastrointestinal structure and function.Br J Surg 1997;84:1425-1429.
[13] Chiu CJ,Mcardle AH,et a1.Intestinal mucoslesion in low flow states.A morphologic hemodynamic and metabolic reappraisa1.Arch Surg,1970,101:478-483.
[14] Takala I.Determinants of splanchnic blood flow.Br J Anaesth 1996,77:50-58
[15] Hinnebusch BF,Ma Q,Henderson J W,et a1.Enterocyte response to ischemia is dependent on differentiation state.J Gastrointest Surg,2002,6(3):403-409
[16]刘海光,杜丹,伦明辉,等.缺血再灌注损伤降低肠粘膜屏障功能的初步研究[J].大连医科大学学报,2004,246(1):l7-19.
[17] Calvet X,Baigorri F,Duarte M, et a1.Effect of sucralfateon gastric intramucosal PH in critically ill patients.Intensive Care Med,1997,23:738-742
[18]华鲁纯,孟淑美,杨俭,等.小肠缺血再灌注损伤时自由基清除剂及MDA变化的实验研究.中国微循环,1999,11(3):205-207.
[19] RuizGines JA,LopezOngil S,GonzalezRubio M,et a1.Reative oxygen species induce proliferation of bovine aortic endothelial cells[J].J Cardiovasc Pharmacol,2000,35(1):109-113.
[20]毛新俊,胡振快,文俊,等.异丙酚对兔小肠缺血再灌注损伤的保护作用.中华麻醉学,2005,9:704-705.
[21] Pelsers MM, Hemtens WT, Glatz JF. Fatty acid binding proteins as plasma markm of itssue injury. Clinic him Acta, 2005, 352(1 -2):15-35.
[22]沈涤华,施诚仁,吴燕,等.肠脂肪酸结合蛋白在肠缺血早期诊断的意义中华麻醉学,2004,25(2):176-178.
[23]刘牧林,张嘉,刘瑞林,等.肠脂肪酸结合蛋白和D-乳酸早期诊断肠缺血-再灌注损害的实验研究.中华创作杂志,2006,22(10):767-770.
[24] Nakatani T,Saito Y,Sakura S et a1.Haemodynamic effects of thoracic epidural anaesthesia during induction of anaesthesia:an investigation into the effects of tracheal intubatien during target-controlled infusion of propofo1.Anaesthesia,2005,60(1):530-536.
[25] Kolkman J,Steverink PJ,Groeneveld AB,et a1.Characteristics of time dependent PCO2 tonomotry in the normal human stomach.Br J naesth,l998,81:669-675.
[26] Cheng YJ,Wang YP,Chien CT,et a1.Small-dose pmpofol sedation attenuates the formation of reactive oxygen species in tourniquet-induced isehemia-repeffusion injury under spinal anesthesia[J].Anesth A nalg,2002,94(6):16-22.
[27] Murphy PG.Myers DS,Davies MJ,et a1.The antioxidant potential of propofol(2,6-dissopropylpheno1).Br J Aanesth,1992,68:613-618.
[28]王亚平,常业恬,钟林.异丙酚对过氧化氢所致的血管内皮细胞损伤的保护作用.中华麻醉学杂志,1998,l8:165-168.
[29] Taniguchi T,kanakura H,kamamoto k,Y effects of posttreatment with propofol on mortality and cytokine responses to endotoxin-induced shock in rats.Crit Care Med ,2002,30:904-907.
[1] Goteri G,Lucarini G,Pieramici T,et al.Endothelial cell Survivin is involved in the growth of ovarian endometriotic cyst[J].Anticancer Res,2005,(6B):4313-4318.
[2] Yang-Z J,Bosco G,Montante A,et a1.Hyperbaric 02 reduce intestinal ischemia reperfusion induced TNF-alpha production and lung neutrophic sequestration[J].Eur J Appl Physic1.2001,85(12):96.
[3] De Souza DA,Greene LJ.Intestinal permeability and systemic infections in critically ill patients.Effect lf glutamine[J].crit Care MED,2005,33(5):1125-113 5.
[4] RuizGines JA,LopezOngil S,GonzalezRubio M,et a1.Reative oxygen species induce proliferation of bovine aortic endothelial cells[J].J Cardiovasc Pharmacol,2000,35(1):109-113.
[5] Castedo E,Segovia J,Escudero C,et al.Ischemia-reperfusion injury during experimental heart transplantation:evaluation of trimetazidineps cytoprotective effect[J].Rev Esp Cordial,2005,58(8):941-950.
[6]王长友,等.复方丹参对肠缺血再灌注损伤防治作用的实验研究[J].中华实用中西医杂志,2005,18(16):677-679.
[7]刘金保,冉丕鑫.粘附分子在缺血再灌注损伤中的作用[J].国外医学生理、病理科学与临床分册,1997,17(3):247.
[8]吕艺,盛志勇,黎君友,等肠缺血再灌注大鼠小肠血管内皮细胞ICAM-1表达的变化及其与肠损伤的关系[J].中华普通外科杂志.2000,15(3):145.
[9] Gross GJ,Kersten JR,Warltier DC.Mechanisms of postischemic contractile dysfunction[J].Ann Thorac Surg,1999,68(5):1898-1904.
[10]张润峰,李霞.丹参改善缺血再灌注血液流变学异常的作用机制研究[J].华西医学,2004,19(2):341-342.
[11] Ikeda H,suzuki Y,Suzuki M,et a1.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.
[12]徐斌,李琳,等活血清下法在小肠缺血再灌注时对细胞凋亡因子Apaf-1和Bcl-2的调控作用[J].天津医学,2007,35(8):598-599.
[13] W u B,Ootani A,Iwakiri R,Fujise T,Tsunada S,Toda S,Fujimoto K.Ischemic preconditioning attenuates ischemia-reperfusion-Induced mucosal apoptosis by inhibiting the mitochondria-dependent pathway in rat small intestine.AmJ Physiol Gastrointest Liver Physiol 2004;286:G580-587.
[14]林世清,黄文起,等.缺血后处理对兔小肠缺血再灌注损伤的影响[J].中华麻醉学,2007,27(11):1042-1044.
[15] Gateau-Roesch O,Argaud L,Ovize M.Mitochondrial permeability transition pore and postconditioning [J].Cardiovasc Res,2006,70(2):264-273.
[16] Argaud L,Gateau-Roesch O,Raisky O,et al.Postconditioning inhibits mitochondrial permeability transition [J].Circulation,2005,111(2):194-197.
[17]褚薇薇,武步强,等.缺血后处理对大鼠肠缺血再灌注损伤肠粘膜细胞线粒体的影响[J].西安交通大学学报,2008,29(14):409-411.
[18] Sola A,Alfaro V,Pesguero J, et al.Co2 in static mesenteric venous blood during intestinal ischemia and ischemic priconditioning in rast [J].shock,2001,16(5):403-408.
[19] Kojima M,Iwakiri R,wu B,et a1.Effects of antioxidative agents on apoptosis induced by ischaemia-reperfusion in rat intestinal mucosa[J].Aliment Pharmacol Ther,2003,18(Suppl 1):139-145.
[20] Sun Z,Olanders K,Lasson A,et a1.Effective treatment of gut barrier dysfunction using an antioxidant,a PAF inhibitor,and monoelonal antibodies against the adhesion molecule PECAM-1 [J].J Surg Res,2002,105(2):220-233.
[21] Ilhan H,Alatas O,Tokar B,et a1.Effects of the anti-ICAM-1 monoclonal antibody,allopurinol,and methylehe blue on intestinal reperfusion injury[J].J Pediatr Surg,2003,38(11):1591-1595.
[22]张华,陈聪德,等.红花对兔肠缺血再灌注损伤后肠壁ICAM-1表达的影响[J].中国中医医结合外科,2009,15(2) :170-173.