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低血糖激活胃泌素和胃酸分泌过程中的特定β-肾上腺素能机制。

Specific beta-adrenergic mechanisms in the hypoglycaemic activation of gastrin and gastric acid secretion.

作者信息

Christensen K C

出版信息

Scand J Gastroenterol. 1984 May;19(3):339-42.

PMID:6377465
Abstract

To study whether specific beta-adrenergic mechanisms contribute to the hypoglycaemic activation of gastrin and gastric acid secretion, the effects of racemic and dextroisomer propranolol (0.1 mg/kg, intravenously) were studied during insulin tests (0.2 IU/kg) in 13 persons. dl-Propranolol inhibited the gastrin response to hypoglycaemia markedly and more than the insignificant alteration observed after d-propranolol. Gastric acid response to hypoglycaemia was significantly reduced by dl-propranolol and not by d-propranolol. The findings demonstrate that non-beta-adrenergic effects of propranolol on the stomach are minor and that specific beta-adrenergic mechanisms are directly or indirectly involved in the hypoglycaemic stimulation of the stomach.

摘要

为研究特定的β-肾上腺素能机制是否促成低血糖对胃泌素和胃酸分泌的激活作用,对13名受试者在进行胰岛素试验(0.2 IU/kg)期间给予消旋和右旋异构体普萘洛尔(0.1 mg/kg,静脉注射),观察其效应。消旋普萘洛尔显著抑制了对低血糖的胃泌素反应,且抑制程度大于右旋普萘洛尔后观察到的轻微变化。消旋普萘洛尔显著降低了对低血糖的胃酸反应,而右旋普萘洛尔则无此作用。这些发现表明,普萘洛尔对胃的非β-肾上腺素能效应较小,且特定的β-肾上腺素能机制直接或间接参与了低血糖对胃的刺激作用。

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