摘要
过量的布比卡因可抑制心脏的传导及收缩功能,而临床上发现布比卡因中毒时肾上腺素的应用会加重其心脏毒性,但发生机制尚不清楚.本文回顾近年的文献报道,综述β肾上腺素受体的激活加重布比卡因心肌毒性的原因及机制.
Excessive bupivacaine inhibits the conduction and contractive function of the heart.Application of epinephrine in bupivacaine poisoning may aggravate the cardiac toxicity,but the mechanism is still unclear.In this paper,the causes and mechanisms of activating beta-adrenergic receptor to aggravate bupivacaine myocardial toxicity are reviewed in recent literatures.
作者
张颖颖
夏登云
Zhang Yingying;Xia Dengyun(Department of Anesthesiology,The First Affiliated Hospital of Hebei North University,Zhangjiakou City,Hebei Province 075000,China)
出处
《实用疼痛学杂志》
2018年第5期389-395,共7页
Pain Clinic Journal
关键词
肾上腺素能Β激动剂
布比卡因
线粒体
离子通道
活性氧
Adrenergic beta-agonists
Bupivacaine
Mitochondria
Ion channels
Reactive oxygen species
作者简介
通信作者:夏登云,Email:xdy9052@163.com
