Bojö L, Cassuto J
Department of Internal Medicine, University of Göteborg, Sweden.
J Auton Nerv Syst. 1992 Apr;38(1):57-64. doi: 10.1016/0165-1838(92)90216-4.
Previous studies in human volunteers have demonstrated an inhibition of gastric motility following painless rectal distension. In the present study we investigated, in anaesthetized rats, the effects of colonic distension on gastric tone and looked at certain aspects of the underlying nervous mechanisms. Changes in gastric volume were monitored continuously by a volumetric method. Colonic distension induced an immediate and pronounced gastric relaxation which lasted throughout the period of distension. The inhibition of gastric tone following colonic distension was abolished by hexamethonium or by bilateral cervical vagotomy. The selective adrenergic alpha 1 blocker, prazosin, the alpha 2 blocker, yohimbine, and the non-selective beta-blocker, propranolol, had no significant effect on gastric relaxation following colonic distension. Likewise, naloxone, an opioid receptor antagonist, did not significantly influence gastric reflex inhibition. It is concluded that colonic distension induced a non-adrenergic inhibition of gastric tone mediated through the vagal nerves. Ganglionic receptors are also suggested to form part of the inhibitory pathway.
先前在人类志愿者身上进行的研究表明，无痛性直肠扩张后胃动力会受到抑制。在本研究中，我们在麻醉大鼠身上研究了结肠扩张对胃张力的影响，并观察了潜在神经机制的某些方面。通过容积法连续监测胃容积的变化。结肠扩张引起了立即且明显的胃松弛，这种松弛在扩张期间持续存在。结肠扩张后胃张力的抑制可被六甲铵或双侧颈迷走神经切断术消除。选择性肾上腺素能α1受体阻滞剂哌唑嗪、α2受体阻滞剂育亨宾和非选择性β受体阻滞剂普萘洛尔，对结肠扩张后的胃松弛没有显著影响。同样，阿片受体拮抗剂纳洛酮也没有显著影响胃反射抑制。得出的结论是，结肠扩张通过迷走神经介导对胃张力产生非肾上腺素能抑制作用。神经节受体也被认为是抑制途径的一部分。
