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肾上腺素诱发大鼠心律失常的机制涉及局部胆碱能激活。

Mechanism of epinephrine-induced dysrhythmias in rat involves local cholinergic activation.

作者信息

Igić R

机构信息

Department of Anesthesiology and Pain Management, Cook County Hospital, Chicago, IL 60612, USA.

出版信息

Can J Physiol Pharmacol. 1996 Jan;74(1):85-8.

PMID:8963956
Abstract

Alterations of autonomic tone can induce cardiac dysrhythmias. In the present experiments intravenous administration of epinephrine (15 micrograms/kg) caused dysrhythmias in rat hearts. Bilateral vagotomy or yohimbine treatment did not suppress the dysrhythmic effects of epinephrine. Atropine, glycopyrrolate, and pertussis toxin reduced the number of premature ventricular contractions and eliminated missed beats caused by epinephrine. Neostigmine increased the number of missed beats but did not change the number of premature ventricular contractions. These results indicate that epinephrine induces cardiac dysrhythmias in part by local release of acetylcholine. Muscarinic receptors and pertussis toxin sensitive G proteins are involved in epinephrine-induced arrhythmogenesis.

摘要

自主神经张力的改变可诱发心律失常。在本实验中,静脉注射肾上腺素(15微克/千克)可导致大鼠心脏出现心律失常。双侧迷走神经切断术或育亨宾治疗并不能抑制肾上腺素的致心律失常作用。阿托品、格隆溴铵和百日咳毒素减少了室性早搏的数量,并消除了由肾上腺素引起的漏搏。新斯的明增加了漏搏的数量,但没有改变室性早搏的数量。这些结果表明,肾上腺素部分通过局部释放乙酰胆碱诱发心律失常。毒蕈碱受体和百日咳毒素敏感的G蛋白参与了肾上腺素诱导的心律失常发生。

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