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胃酸分泌和血流量在迷走神经刺激诱导胃黏膜损伤发生中的作用。

Role of gastric acid secretion and blood flow in the development of vagal stimulation induced gastric mucosal damage.

作者信息

Hierlihy L E, Wallace J L, Ferguson A V

机构信息

Department of Physiology, Queen's University, Kingston, ON, Canada.

出版信息

Can J Physiol Pharmacol. 1993 Oct-Nov;71(10-11):829-34. doi: 10.1139/y93-124.

DOI:10.1139/y93-124
PMID:8143242
Abstract

Vagal stimulation has been shown to result in the development of gastric mucosal erosions in the rat, although the mechanisms underlying the development of such erosions are not known. The effects of vagal stimulation on gastric acid secretion and mucosal blood flow were examined in urethane-anesthetized male Sprague-Dawley rats to determine whether changes in these factors correlate with the mucosal damage in response to vagal stimulation. Electrical stimulation (5 Hz, 5 V, 1 ms for 60 min) of afferent or efferent components of the vagi was not found to induce any significant increase in the mean acid secretory rate compared with control animals (p > 0.05). In contrast, stimulation of intact vagus nerves induced a significant increase in the mean acid secretory rate compared with control and efferent- and afferent-stimulated groups (p < 0.01). Measurement of gastric blood flow with laser-Doppler flowmetry demonstrated intact vagal stimulation to have no significant effect on gastric blood flow. These data suggest that such vagal stimulation induced increases in acid secretion in urethane-anesthetized animals may represent a part of the integrated physiological response to such stimulation which leads to the development of gastric mucosal erosions within 60 min. Pretreatment with antisecretory agents such as cimetidine and interleukin-1 beta significantly reduce the gastric mucosal injury compared with untreated animals (p < 0.05), emphasizing the important role of acid secretion in the development of vagal-induced gastric damage.

摘要

迷走神经刺激已被证明会导致大鼠胃黏膜糜烂,尽管这种糜烂发生的潜在机制尚不清楚。在氨基甲酸乙酯麻醉的雄性斯普拉格-道利大鼠中,研究了迷走神经刺激对胃酸分泌和黏膜血流量的影响,以确定这些因素的变化是否与迷走神经刺激引起的黏膜损伤相关。与对照动物相比,对迷走神经传入或传出成分进行电刺激(5Hz,5V,1ms,持续60分钟)未发现平均胃酸分泌率有任何显著增加(p>0.05)。相比之下,与对照组以及传出和传入刺激组相比,完整迷走神经刺激使平均胃酸分泌率显著增加(p<0.01)。用激光多普勒血流仪测量胃血流量表明,完整迷走神经刺激对胃血流量无显著影响。这些数据表明,在氨基甲酸乙酯麻醉的动物中,这种迷走神经刺激引起的胃酸分泌增加可能是对这种刺激的综合生理反应的一部分,这种反应会在60分钟内导致胃黏膜糜烂。与未治疗的动物相比,用西咪替丁和白细胞介素-1β等抗分泌剂预处理可显著减轻胃黏膜损伤(p<0.05),强调了胃酸分泌在迷走神经诱导的胃损伤发生中的重要作用。

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