title: Role of endogenous opioid peptides in protection of ischemic preconditioning in rat small intestine.
abstract: 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.
authors.affiliation: Department of Pharmacology, Shanxi Medical University, Taiyuan, PR China.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: Y X
authors.initials: YX
authors.lastname: Wu
authors.forename: Y B
authors.initials: YB
authors.lastname: Hao
authors.forename: Y
authors.initials: Y
authors.lastname: Dun
authors.forename: S P
authors.initials: SP
authors.lastname: Yang
mesh_terms: D000701:Analgesics, Opioid / Q000037:antagonists & inhibitors / Q000494:pharmacology; D000818:Animals; D004347:Drug Interactions; D004487:Edema / Q000209:etiology / Q000517:prevention & control; D004743:Enkephalin, Leucine / Q000378:metabolism; D007410:Intestinal Diseases / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control; D007413:Intestinal Mucosa / Q000473:pathology; D007421:Intestine, Small / Q000098:blood supply* / Q000473:pathology / Q000502:physiology; D007511:Ischemia / Q000378:metabolism; D019194:Ischemic Preconditioning; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009020:Morphine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D018847:Opioid Peptides / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D011957:Receptors, Opioid / Q000502:physiology; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control
chemical_list: D000701:Analgesics, Opioid; D009292:Narcotic Antagonists; D018847:Opioid Peptides; D011957:Receptors, Opioid; D009270:Naloxone; D008315:Malondialdehyde; D004743:Enkephalin, Leucine; D009020:Morphine; D007770:L-Lactate Dehydrogenase