Bojö L, Lefebvre R A, Nellgård P, Cassuto J
Department of Physiology, University of Göteborg, Sweden.
Eur J Pharmacol. 1993 Jun 4;236(3):443-8. doi: 10.1016/0014-2999(93)90483-x.
We have previously presented evidence for a non-adrenergic, vagally mediated colono-gastric inhibitory reflex induced by distension of the colon. We also found that pain stimulation by putting pressure on a testicle induced a pronounced gastric relaxation mediated by both adrenergic and vagal non-adrenergic fibres in anesthetized rats. Previous in vitro studies by other workers have strongly indicated that vasoactive intestinal polypeptide (VIP) is a neural mediator of gastric relaxation. The aim of the present in vivo study was to investigate, in anesthetized rats, whether VIP is involved in the gastric reflex relaxation induced by colonic distension and pain stimulation. A volumetric method was used to monitor changes in gastric volume. Gastric reflex relaxation following colonic distension was significantly and markedly inhibited by VIP antiserum as compared to the control relaxation before administration of the antiserum. Non-immunized control serum did not significantly influence gastric relaxation caused by colonic distension. Pain-induced gastric relaxation was moderately but significantly reduced after the administration of VIP antiserum but not after control serum. The selective beta 2-adrenoceptor agonist, salbutamol, induced a pronounced gastric relaxation of the same magnitude before and after the administration of VIP antiserum. VIP antiserum changed the pattern of gastric motility by inducing a specific type of gastric contraction appearing spontaneously or in response to colonic distension. A close intra-arterial injection of VIP induced gastric relaxation and inhibition of phasic gastric contractions. The present results in the rat suggest that VIP or a VIP-like peptide is involved in gastric reflex relaxation induced by colonic distension and pain stimulation.
我们之前已经提出证据，证明结肠扩张可诱发一种由迷走神经介导的非肾上腺素能性结肠 - 胃抑制反射。我们还发现，在麻醉大鼠中，按压睾丸引起的疼痛刺激可诱发由肾上腺素能纤维和迷走神经非肾上腺素能纤维介导的显著胃舒张。其他研究人员之前的体外研究强烈表明，血管活性肠肽（VIP）是胃舒张的神经介质。本体内研究的目的是在麻醉大鼠中研究VIP是否参与结肠扩张和疼痛刺激诱发的胃反射性舒张。采用容积法监测胃容积的变化。与给予抗血清前的对照舒张相比，VIP抗血清可显著且明显抑制结肠扩张后的胃反射性舒张。未免疫的对照血清对结肠扩张引起的胃舒张无显著影响。给予VIP抗血清后，疼痛诱导的胃舒张有适度但显著的降低，而给予对照血清后则无此现象。选择性β2 - 肾上腺素能受体激动剂沙丁胺醇在给予VIP抗血清前后诱导出相同程度的显著胃舒张。VIP抗血清通过诱导自发出现或对结肠扩张作出反应的特定类型的胃收缩，改变了胃运动模式。动脉内近距离注射VIP可诱导胃舒张并抑制胃的相性收缩。目前在大鼠中的研究结果表明，VIP或一种VIP样肽参与结肠扩张和疼痛刺激诱发的胃反射性舒张。
