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观察预适应对大鼠小肠缺血再灌的保护作用及对内源性神经递质降钙素基因相关肽 (CGRP)释放的影响 .选用雄性 Wistar大鼠 40只 (2 75- 32 5g) ,实验分在体和离体两部分 .(1 )在体部分 :30 min的小肠缺血和 60 min的再灌流可引起小肠湿重干重比值 (WW/DW)增高 ,血中乳酸脱氢酶 (LDH)活性 ,丙二醛 (MDA)含量显著增加 .3次 8min缺血及1 0 min再灌流预适应可降低前述缺血再灌引起的WW/DW,LDH活性及 MDA含量增高 ,但各组血液中 CGRP水平未见明显变化 .(2 )离体部分 :肠系膜上动脉插管连接灌流装置 .肠系膜上静脉插管收集流出液 .小肠灌流 1 0 min后 ,反复 3次 8min阻断灌流及 1 0 min再灌流预适应模型可使流出液中的 CGRP显著增加〔(1 .30± 0 .0 8) vs(0 .68±0 .0 5) μg· L-1,P<0 .0 1〕.结果提示 :缺血预适应对小肠缺血再灌损伤具有显著保护作用 ,CGRP可能是预适应的一种内源性神经介质
To observe the protective effect of preconditioning on intestinal ischemia-reperfusion in rats and its effect on the release of calcitonin gene-related peptide (CGRP), an endogenous neurotransmitter.Methods Forty male Wistar rats (2 75-32 5 g) The experiment was divided into two parts: in vivo and in vitro. (1) In the body part, intestinal ischemia at 30 min and reperfusion at 60 min caused an increase in the ratio of wet / dry weight of small intestine (WW / DW), lactate dehydrogenase (LDH) activity and malondialdehyde (MDA) content increased significantly.33minutes 8min ischemia and 10min reperfusion preconditioning can reduce the above-mentioned activity of WW / DW, LDH and MDA content increased after ischemia-reperfusion, (2) Ex vivo: superior mesenteric artery was cannulated and connected with perfusion device, superior mesenteric vein catheter was used to collect effluent, and after 10 min of small intestine perfusion, repeated 3 times for 8 min to block perfusion and The reperfusion preconditioning model at 10 min could significantly increase the CGRP in the effluent [(1.30 ± 0.08) vs (0.68 ± 0.05) μg · L-1, P <0 .0 1〕 .The results suggest that: ischemic preconditioning has a significant protective effect on intestinal ischemia-reperfusion injury, CGRP may be a preconditioning of an endogenous nerve mediator