Midazolam in rabbits terminates dysrhythmias caused by intracerebroventricular ropivacaine

作     者：Yao-min ZHU Zu-yi YUAN Hui WU Dan-dan ZHOU Gui-xia JING 

作者机构：Department of Anesthesiology the First Affiliated Hospital School of Medicine Xi 'an Jiaotong University Xi 'an 710061 China Department of Cardiology the First Affiliated Hospital School of Medicine Xi 'an Jiaotong University Xi 'an 710061 China 

出 版 物：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 (浙江大学学报（英文版）B辑（生物医学与生物技术）)

年 卷 期：2011年第12卷第8期

页      面：668-676页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Project (No. 2006K13-G7-4) supported by the Key Sci-Tech Research Project of Shaanxi Province China 

主　　题：Ropivacaine Cardiotoxicity Ventricular cerebrospinal fluid Central nervous system (CNS) Dysrhythmias Midazolam 

摘      要：The current study was designed to investigate the mechanisms by which ropivacaine may act within the central nervous system （CNS） to produce cardiotoxicity. Eighty New Zealand rabbits were divided into four groups randomly. In Group 1,20 rabbits received intracerebroventricular （icv） saline, and then received icv ropivacaine 30 min later. In Group 2, 20 rabbits received icv ropivacaine. Whenever dysrhythmias continued for more than 5 min, 0.1 ml saline was administered into the left cerebral ventricle. Ten minutes later, 0.1 ml midazolam was given into the left lateral ventricle. In Group 3, 20 rabbits received icv ropivacaine, and once the dysrhythmias developed, the inspired isoflurane concentration was increased from 0.75% to 1.50%. In Group 4, 20 animals received an intravenous （iv） phenylephrine infusion until dysrhythmias occurred. In Group 1, the rabbits did not develop dysrhythmias in response to icv saline, whereas dysrhythmias did develop in these animals after icv ropivacaine. In Group 2, icv saline had no effect on the dysrhythmias; however, icv midazolam terminated cardiac dysrhythmias. In Group 3, an increase in the concentration of the inspired isoflurane had no effect on dysrhythmias. In Group 4, icv midazolam had no effect on dysrhythmias in response to iv phenylephdne. Ropivacaine administered directly into the CNS is capable of producing cardiac dysrhythmias; midazolam terminated dysrhythmias presumably by potentiation of y-aminobutyric acid （GABA） receptor activity. Our results suggest that ropivacaine produces some of its cardiotoxicity not only by the direct cardiotoxicity of the drug, but also by the CNS effects of ropivacaine.