Release of vasodilator, but not vasoconstrictor, neuropeptides and of enteroglucagon by intestinal ischaemia/reperfusion in the rat.
Release of vasodilator, but not vasoconstrictor, neuropeptides and of enteroglucagon by intestinal ischaemia/reperfusion in the rat.
复制标题
大鼠肠缺血/再灌注释放血管舒张剂，但不释放血管收缩剂、神经肽和肠高血糖素。
作者：
L. Meleagros;M. Ghatei;S. Bloom
肠缺血再灌注的特点是最初的充血和随后的粘膜修复。这项研究调查了肠道血管活性神经肽和营养多肽在这些现象中的可能作用。各组大鼠在肠系膜上动脉阻断期间监测5或20分钟，有或没有随后再灌注5分钟。用放射免疫法测定动脉血中的多肽浓度(fmoL/ml)。单独的肠缺血不会引起血流动力学障碍或多肽释放。缺血5分钟后再灌流，导致动脉低血压和血浆血管活性肠多肽升高(37(3)，对照组11(4)，p<；0.001)。在缺血20分钟后，再灌流导致更大的低血压(p<；0.05)和释放血管活性肠多肽(31(3)，p<；0.05v对照)和更有效的血管扩张剂β-降钙素基因相关肽(49(3)，对照23(1)，p<；0.001)。相比之下，血管扩张剂α-降钙素基因相关肽和P物质以及血管收缩因子神经肽Y、肽YY和生长抑素未被释放。缺血再灌流20min后释放刺激性神经肽蛙皮素(13(2)，对照7(3)，p<；0.05)。血浆肠高血糖素在缺血/再灌注5分钟和20分钟后从对照组(51(4))上升到110(16)(p<；0.001)和158(27)(p<；0.005)。强大的肠血管扩张剂血管活性肠肽和β-降钙素基因相关肽可能促进缺血后肠充血，而不被血管收缩药所对抗。血浆肠高血糖素的升高可能表明弥漫性粘膜损伤，并与这种多肽的营养作用相一致。
Reperfusion of ischaemic intestine is characterised by an initial hyperaemia with ensuing mucosal repair. This study investigated possible roles for gut vasoactive neuropeptides and trophic peptides in these phenomena. Groups of rats were monitored during superior mesenteric artery occlusion for five or 20 minutes, with or without subsequent reperfusion for five minutes. Peptide concentrations (fmol/ml) in arterial blood, were measured using specific radioimmunoassays. Intestinal ischaemia alone did not cause haemodynamic disturbance or peptide release. Reperfusion, after five minutes of ischaemia, resulted in arterial hypotension and a rise in plasma vasoactive intestinal polypeptide (mean (SEM)) (37 (3), control 11 (4), p < 0.001). After 20 minutes of ischaemia, reperfusion resulted in greater hypotension (p < 0.05) and release of both vasoactive intestinal polypeptide (31 (3), p < 0.05 v control) and the more potent vasodilator beta-calcitonin gene related peptide (49 (3), control 23 (1), p < 0.001). By contrast, the vasodilators alpha-calcitonin gene related peptide and substance P and the vasoconstrictors neuropeptide Y, peptide YY, and somatostatin were not released. Bombesin, a stimulatory neuropeptide, was released after 20 minutes of ischaemia/reperfusion (13 (2), control 7 (3), p < 0.05). Plasma enteroglucagon rose from control (51 (4)) to 110 (16) (p < 0.001) and to 158 (27) (p < 0.005) after five and 20 minutes of ischaemia/reperfusion. The potent enteric vasodilators vasoactive intestinal polypeptide and beta-calcitonin gene related peptide, unopposed by vasoconstrictors, may promote post-ischaemic intestinal hyperaemia. The rise in plasma enteroglucagon may point to diffuse mucosal injury and is consistent with the putative trophic role of this peptide.
组胺：肠缺血/再灌注中黄嘌呤氧化酶活性的促进剂。
影响因子：
2.4
作者：
Caty,MG;Schmeling,DJ;Friedl,HP;Oldham,KT;Guice,KS;Till,GO
通讯作者：
Till,GO
内脏动脉闭塞休克期间肾上腺和肠道分泌儿茶酚胺和神经肽。
DOI：
--
发表时间：
1988
期刊：
Circulatory shock
影响因子：
--
作者：
Gaumann,DM;Yaksh,TL
通讯作者：
Yaksh,TL