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在麻醉犬中,短暂迷走神经刺激后一氧化氮介导胃舒张。

NO mediates gastric relaxation after brief vagal stimulation in anesthetized dogs.

作者信息

Meulemans A L, Eelen J G, Schuurkes J A

机构信息

Department of Gastrointestinal Pharmacology, Janssen Research Foundation, Beerse, Belgium.

出版信息

Am J Physiol. 1995 Aug;269(2 Pt 1):G255-61. doi: 10.1152/ajpgi.1995.269.2.G255.

DOI:10.1152/ajpgi.1995.269.2.G255
PMID:7653566
Abstract

In vitro studies showed that relaxations induced after vagal stimulation of the guinea pig stomach are mediated via nitric oxide (NO). The role of NO in canine gastric relaxation in response to vagal stimulation has as yet not been studied. The present study examined the influence of NG-nitro-L-arginine (L-NNA) on gastric relaxations after vagal nerve stimulation in the anesthetized dog. In beagle dogs (n = 7), the ventral and dorsal abdominal vagal nerves were connected to a pair of platinum electrodes. Gastric tone was measured by means of a barostat. Changes in gastric motility were measured with force transducers sutured on the fundus and the antrum. The cervical vagi were sectioned, and dogs were given atropine (0.2 mg/kg i.v.) and guanethidine (5 mg/kg i.v.). Electrical stimulation of the vagal trunks (19 V, 1-ms duration, for 15 s every 2 min, 1-30 Hz) induced frequency-dependent increases in volume. On the fundus, frequency-dependent relaxations could be observed (maximal effect at 5 mmHg and at 10 Hz). During electrical stimulation, the spontaneous antral contractions were completely blocked. After cessation of the stimulus, "rebound" contractions could be observed. L-NNA (5 mg/kg i.v.) completely blocked the increases in gastric volume and the relaxations on the fundus. On the antrum, however, contractions were observed during the electrical stimulation. L-Arginine (250 mg/kg i.v.) gradually restored the relaxations on electrical stimulation. This study demonstrates that NO mediates short-lasting vagally induced gastric relaxations in the anesthetized dog.

摘要

体外研究表明,豚鼠胃迷走神经刺激后诱导的舒张是通过一氧化氮(NO)介导的。NO在犬迷走神经刺激引起的胃舒张中的作用尚未得到研究。本研究检测了NG-硝基-L-精氨酸(L-NNA)对麻醉犬迷走神经刺激后胃舒张的影响。在比格犬(n = 7)中,腹侧和背侧腹部迷走神经连接到一对铂电极。通过压力传感器测量胃张力。用缝合在胃底和胃窦的力传感器测量胃动力的变化。切断颈迷走神经,给犬静脉注射阿托品(0.2 mg/kg)和胍乙啶(5 mg/kg)。迷走神经干电刺激(19 V,持续1 ms,每2分钟刺激15 s,频率1 - 30 Hz)引起容积的频率依赖性增加。在胃底,可观察到频率依赖性舒张(在5 mmHg和10 Hz时达到最大效应)。电刺激期间,胃窦自发性收缩完全被阻断。刺激停止后,可观察到“反弹”收缩。静脉注射L-NNA(5 mg/kg)完全阻断了胃容积的增加和胃底的舒张。然而,在胃窦,电刺激期间观察到收缩。静脉注射L-精氨酸(250 mg/kg)逐渐恢复了电刺激时的舒张。本研究表明,NO介导麻醉犬中迷走神经诱导的短暂胃舒张。

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