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低血容量通过α-2肾上腺素能机制抑制大鼠十二指肠中酸诱导的碱转运。

Hypovolaemia inhibits acid-induced alkaline transport in the rat duodenum via an alpha-2 adrenergic mechanism.

作者信息

Jönson C, Hamlet A, Fändriks L

机构信息

Department of Physiology, University of Göteborg, Sweden.

出版信息

Acta Physiol Scand. 1991 Jul;142(3):367-73. doi: 10.1111/j.1748-1716.1991.tb09170.x.

Abstract

Acid exposure of the duodenal mucosa is a well-known stimulant of the mucosal alkaline secretion. We have previously reported that a minor blood loss inhibits this secretory increment via activation of the splanchnic nerves. In the present study the pharmacological characteristics of the splanchnic neural inhibition of the alkaline secretion were investigated. Duodenal HCO3- secretion was measured by in-situ titration in chloralose-anaesthetized rats. Exposure of the duodenal mucosa to hydrochloric acid (0.01 M, 5 min) increased the secretion by approximately 60%. A 10% decrease in blood volume simultaneously to the luminal acidification abolished the secretory increase, as previously reported. Treatment with either guanethidine or yohimbine blocked the bleeding-induced inhibition of the secretion after acid-exposure. Neither prazosin nor propranolol did prevent such hypovolaemia-induced inhibition of duodenal alkaline secretion. The present results suggest that the splanchnic neural inhibition of acid-induced duodenal HCO3- secretion is mediated via adrenergic nerve fibres and alpha-2 adrenoceptors.

摘要

十二指肠黏膜暴露于酸性环境是黏膜碱性分泌的一种众所周知的刺激因素。我们之前曾报道,少量失血会通过激活内脏神经来抑制这种分泌增加。在本研究中,对内脏神经对碱性分泌的抑制作用的药理学特性进行了研究。通过在水合氯醛麻醉的大鼠中进行原位滴定来测量十二指肠HCO₃⁻分泌。将十二指肠黏膜暴露于盐酸(0.01 M,5分钟)可使分泌增加约60%。如先前报道,在管腔酸化的同时血容量减少10%会消除分泌增加。用胍乙啶或育亨宾处理可阻断酸暴露后出血诱导的分泌抑制。哌唑嗪和普萘洛尔均不能预防这种低血容量诱导的十二指肠碱性分泌抑制。目前的结果表明,内脏神经对酸诱导的十二指肠HCO₃⁻分泌的抑制是通过肾上腺素能神经纤维和α₂肾上腺素能受体介导的。

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