Zhang Y, Wu Y X, Hao Y B, Dun Y, Yang S P
Department of Pharmacology, Shanxi Medical University, Taiyuan, PR China.
Life Sci. 2001 Jan 19;68(9):1013-9. doi: 10.1016/s0024-3205(00)01004-3.
This study investigated the protective effects of ischemic preconditioning on intestinal ischemic injury and the role of endogenous opioid peptides (EOP) in these effects. Ischemia-reperfusion (I/R) induced by 30-min of ischemia and 60-min of reperfusion significantly increased the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and resulted in serious intestinal edema (wet weight/dry weight). The ischemic preconditioning (PC) elicited by three 8-min occlusion periods interspersed with 10-min reperfusion markedly attenuated intestinal injury caused by ischemia-reperfusion. Pretreatment with morphine (300 microg x kg(-1), i.v.) 10-min before ischemia and reperfusion mimicked the protection produced by PC. Naloxone (3 mg x kg(-1), i.v.) abolished the protection of morphine-induced preconditioning and ischemic preconditioning in rat intestine. However, there were no changes between naloxone alone and control groups. Treatment with naloxone before ischemia-reperfusion had no effect on animals compared with the I/R group. In addition, we also measured the content of endogenous opioid peptides (Leu-enkephalin) in the effluent which was collected before and during preconditioning. It was shown that the release of leu-enkephalin was markedly increased during preconditioning. These results suggested that EOP might play an important role in PC in rat small intestine.
本研究探讨了缺血预处理对肠缺血损伤的保护作用以及内源性阿片肽（EOP）在这些作用中的角色。由30分钟缺血和60分钟再灌注诱导的缺血-再灌注（I/R）显著增加了丙二醛（MDA）和乳酸脱氢酶（LDH）的水平，并导致严重的肠水肿（湿重/干重）。由三个8分钟阻断期穿插10分钟再灌注引发的缺血预处理（PC）明显减轻了缺血-再灌注引起的肠损伤。在缺血和再灌注前10分钟静脉注射吗啡（300μg·kg⁻¹）预处理模拟了PC产生的保护作用。纳洛酮（3mg·kg⁻¹，静脉注射）消除了吗啡诱导的预处理和大鼠肠道缺血预处理的保护作用。然而，单独使用纳洛酮组与对照组之间没有变化。与I/R组相比，在缺血-再灌注前用纳洛酮治疗对动物没有影响。此外，我们还测量了预处理前和预处理期间收集的流出物中内源性阿片肽（亮脑啡肽）的含量。结果表明，预处理期间亮脑啡肽的释放明显增加。这些结果表明，EOP可能在大鼠小肠的PC中起重要作用。
