Glise H, Abrahamsson H
Scand J Gastroenterol. 1980;15(6):665-72. doi: 10.3109/00365528009181513.
Reflex inhibition of gastric motility in response to intestinal nociception and afferent nerve stimulation was studied in anesthetized cats. Mechanical stimulation of the small and large intestines elicited marked gastric inhibition, which was imitated by direct electrical stimulation of mesenteric or splanchnic afferents. The reflex response was resistant to atropine, guanethidine, and adrenalectomy. Spinal cord transection at the cervical level or spinal anesthesia completely blocked the reflex, as did vagotomy or vagal cold blockade. Chemical peritoneal stimulation by hydrochloric acid induced long-lasting gastric inhibition, which was not blocked by antiadrenergic or anticholinergic drugs. This response was reduced, but not completely blocked by spinal anesthesia or spinal cord transection. It is concluded that various nociceptive intestinal stimuli suppress gastric motility via a spino-vagal reflex mechanism composed of spinal afferents in the sympathetic nerves, spinobulbar ascending pathways, and vagal nonadrenergic inhibitory fibers to the stomach. In addition, vago-vagal reflexes evidently contribute to the gastric suppression induced by diffuse peritoneal irritation. These two reflex mechanisms are suggested to be mainly responsible for postoperative gastric inhibition, together with sympatho-adrenergic reflexes.
在麻醉猫身上研究了肠道伤害性感受和传入神经刺激引起的胃动力反射抑制。对小肠和大肠的机械刺激引起明显的胃抑制，肠系膜或内脏传入神经的直接电刺激可模拟这种抑制。该反射反应对阿托品、胍乙啶和肾上腺切除术有抗性。颈段脊髓横断或脊髓麻醉完全阻断了该反射，迷走神经切断术或迷走神经冷阻断术也有同样效果。盐酸化学性腹膜刺激引起持久的胃抑制，抗肾上腺素能或抗胆碱能药物不能阻断这种抑制。脊髓麻醉或脊髓横断可使这种反应减弱，但不能完全阻断。结论是，各种伤害性肠道刺激通过一种由交感神经中的脊髓传入神经、脊髓延髓上行通路以及迷走神经至胃的非肾上腺素能抑制纤维组成的脊髓-迷走神经反射机制抑制胃动力。此外，迷走-迷走神经反射显然参与了弥漫性腹膜刺激引起的胃抑制。这两种反射机制与交感-肾上腺素能反射一起，被认为是术后胃抑制的主要原因。
