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出血诱导的大鼠十二指肠HCO3-分泌减少是通过α2肾上腺素能受体介导的。

Bleeding-induced decrease in duodenal HCO3- secretion in the rat is mediated via alpha 2-adrenoceptors.

作者信息

Jönson C, Fändriks L

出版信息

Acta Physiol Scand. 1987 Jul;130(3):387-91. doi: 10.1111/j.1748-1716.1987.tb08153.x.

Abstract

This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO3- secretion. The HCO3- output was measured by in situ titration in a duodenal segment. Blood loss of 0.6 ml per 100 g body wt (approximately 10% of total blood volume) reduced duodenal HCO3- secretion by about 30%. Pretreatment with guanethidine did not affect basal output of HCO3- but markedly reduced the bleeding-induced response. The alpha 2-adrenoceptor antagonist yohimbine did not affect the basal secretion but almost abolished the depression of duodenal HCO3- secretion due to blood loss. Pretreatment with the alpha 1-adrenoceptor antagonist prazosine or the beta-adrenoceptor antagonist propranolol did neither change basal duodenal HCO3- secretion nor the bleeding-induced decrease in duodenal HCO3- secretion. It is suggested that a small blood loss by means of a reflex activation of the sympathetic nervous system, and via the release of transmitter substances from adrenergic nerve endings, reduces the duodenal HCO3- secretion. The inhibitory effect is mainly due to activation of alpha 2-adrenoceptors.

摘要

本研究在水合氯醛麻醉的大鼠身上进行,以检验少量失血对十二指肠HCO₃⁻分泌的影响。通过对十二指肠段进行原位滴定来测量HCO₃⁻的排出量。每100克体重失血0.6毫升(约占总血容量的10%)可使十二指肠HCO₃⁻分泌减少约30%。用胍乙啶预处理不影响HCO₃⁻的基础排出量,但显著降低了出血诱导的反应。α₂肾上腺素能受体拮抗剂育亨宾不影响基础分泌,但几乎消除了由于失血导致的十二指肠HCO₃⁻分泌减少。用α₁肾上腺素能受体拮抗剂哌唑嗪或β肾上腺素能受体拮抗剂普萘洛尔预处理既不改变十二指肠HCO₃⁻的基础分泌,也不改变出血诱导的十二指肠HCO₃⁻分泌减少。提示少量失血通过交感神经系统的反射性激活,并通过肾上腺素能神经末梢释放递质,减少十二指肠HCO₃⁻分泌。抑制作用主要是由于α₂肾上腺素能受体的激活。

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