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内皮素诱导的持久肠系膜血管收缩:非闭塞性肠梗死的一种假说机制。

Endothelin-induced long-lasting mesenteric vasoconstriction: a hypothetical mechanism of non-occlusive intestinal infarction.

作者信息

Dóbi I, Kékesi V, Tóth M, Juhász-Nagy S

机构信息

Department of Cardiovascular Surgery, Semmelweis University Medical School, Budapest, Hungary.

出版信息

Acta Chir Hung. 1991;32(3):199-208.

PMID:1842471
Abstract

The in vivo mesenteric vascular effect of the novel, endothelium-derived endogenous polypeptide, endothelin-1 (ET-1) was examined in experiments performed on pentobarbital-anesthetized dogs. Blood supply to a segment of the small bowel was measured simultaneously with an electromagnetic flow probe and computer-assisted thermography which senses flow-dependent infrared irradiation. It was found that close mesenteric arterial injections of ET-1 produced long-lasting flow decreases of considerable magnitude: the single dose of 1 nmol reduced blood flow by nearly 90 percent, and even the minimal single amount of 1 pmol produced statistically significant vasoconstriction. The thermographic analysis proved the homogenous character of these reactions. Unlike vascular responses elicited by most of the known vasoconstrictive agents, the ET-1-induced spastic effects were maintained without a continuous exposure (drug infusion). All features that characterize the spastic ET-1 action qualify the peptide for a hypothetical candidate of mediating the nonocclusive mesenteric ischemic syndrome.

摘要

在戊巴比妥麻醉的狗身上进行的实验中,研究了新型内皮源性内源性多肽内皮素-1(ET-1)的体内肠系膜血管效应。用电磁流量探头和感应与流量相关的红外辐射的计算机辅助热成像技术同时测量小肠一段的血液供应。结果发现,肠系膜动脉近距离注射ET-1会产生持续时间长且幅度相当大的血流减少:单剂量1 nmol可使血流量减少近90%,即使最小单剂量1 pmol也会产生具有统计学意义的血管收缩。热成像分析证明了这些反应的均匀性。与大多数已知血管收缩剂引起的血管反应不同,ET-1诱导的痉挛效应在没有持续暴露(药物输注)的情况下仍能维持。所有表征ET-1痉挛作用的特征都使该肽成为介导非闭塞性肠系膜缺血综合征的假想候选物。

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