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疼痛引起的胃动力抑制是由大鼠的肾上腺素能和迷走神经非肾上腺素能反射介导的。

Pain-induced inhibition of gastric motility is mediated by adrenergic and vagal non-adrenergic reflexes in the rat.

作者信息

Bojö L, Cassuto J, Nellgård P

机构信息

Department of Internal Medicine, University of Göteborg, Sweden.

出版信息

Acta Physiol Scand. 1992 Nov;146(3):377-83. doi: 10.1111/j.1748-1716.1992.tb09432.x.

DOI:10.1111/j.1748-1716.1992.tb09432.x
PMID:1481692
Abstract

Painful stimuli have been shown to inhibit gastric motility in animal experiments and delay gastric emptying in humans. The aim of the present study was to investigate in detail mechanisms involved in pain-induced gastric inhibition. Pain stimulation by exerting pressure on a testicle induced a prompt gastric relaxation which lasted throughout the period of stimulation. Pain-induced gastric relaxation was significantly reduced by the selective alpha-1 blocker, prazosin, and by the non-selective beta-blocker, propranolol. Similarly pain-induced inhibition of gastric tone was significantly reduced by bilateral cervical vagotomy. In contrast, gastric relaxation following pain stimulation was significantly potentiated by the selective adrenergic alpha-2 blocker, yohimbine. Combined administration of prazosin and propranolol followed by bilateral cervical vagotomy abolished gastric relaxation in response to pain stimulation. In conclusion, gastric relaxation in response to painful stimulation was found to be reflex-mediated via sympathetic neurons acting on alpha-1 and beta receptors and possibly also via vagal non-adrenergic fibres. Pain-induced inhibition of gastric tone was significantly increased by yohimbine. It is suggested that yohimbine by blocking presynaptic inhibitory receptors on adrenergic neurons facilitates the release of noradrenaline in response to pain stimulation.

摘要

在动物实验中,疼痛刺激已被证明会抑制胃动力,在人类中则会延迟胃排空。本研究的目的是详细探究疼痛诱导胃抑制所涉及的机制。通过对睾丸施加压力进行疼痛刺激会引发迅速的胃舒张,这种舒张在整个刺激期间持续存在。选择性α-1受体阻滞剂哌唑嗪和非选择性β受体阻滞剂普萘洛尔可显著减轻疼痛诱导的胃舒张。同样,双侧颈迷走神经切断术可显著减轻疼痛诱导的胃张力抑制。相比之下,选择性肾上腺素能α-2受体阻滞剂育亨宾可显著增强疼痛刺激后的胃舒张。先联合给予哌唑嗪和普萘洛尔,然后进行双侧颈迷走神经切断术,可消除疼痛刺激引起的胃舒张。总之,发现疼痛刺激引起的胃舒张是通过作用于α-1和β受体的交感神经元以及可能还通过迷走神经非肾上腺素能纤维介导的反射。育亨宾可显著增强疼痛诱导的胃张力抑制。提示育亨宾通过阻断肾上腺素能神经元上的突触前抑制性受体,促进了去甲肾上腺素在疼痛刺激时的释放。

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