The Studies on the Epinephrine - Induced Arrhythmias During Halothane Anesthesia in Dogs.
10.4097/kjae.1992.25.2.242
- Author:
Seong Shick SHIN
1
;
Chang Young JEONG
;
In Ho HA
;
Sung Su CHUNG
Author Information
1. Department of Anesthesiology, Chonnam National University Medical School, Kwang-Ju, Korea.
- Publication Type:Original Article
- Keywords:
Halothane;
Arrythmogenic dose of epinephrine;
Prazosin;
Verapamil
- MeSH:
Anesthesia*;
Animals;
Arrhythmias, Cardiac*;
Blood Pressure;
Calcium Channels;
Catecholamines;
Dogs*;
Epinephrine*;
Halothane*;
Heart;
Lidocaine;
Nitroprusside;
Prazosin;
Propranolol;
Verapamil
- From:Korean Journal of Anesthesiology
1992;25(2):242-251
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
It is known that the concurrent administration of epinephrine, whether applied subcutaneously or parenterally during halothane anesthesia, can result in the initiation of ventrieular arrhythmias, which may be life threatening. However the mechanism by which halothane sensitizes the heart to catecholamines are not known yet. The purpose of this study was to investigate the mechanism of epinephrine induced cardiac arrhythmias during 1.2 MAC halothane anesthesia in dogs. Thirty-eight dogs were randomly assigned to five groups, halothane anesthesia were measured the arrythmogenic doses of epinephrine(ADE) before and after each treatment with sodium nitroprusside (SNP) (n=9), lidocaine(n=7), propranolol(n=7), prazosin(n=7) and verapamil(n=8), and compared each other. The results were follows. 1) The control ADE to induce ventricular arrhythmias was 2.160.15 ug/kg/min. 2) Treatment with SNP resulted in a decrease(28%) in mean blood pressure, but did not increase the ADE compared to the control. 3) Lidocaine and propranolol significantly increased the control ADE by 1.5 times, respectively, but there was no different between the ADE of lidocaine and that of propranolol. 4) Prazosin and verapamil also significantly increased the control ADE by 3.3 times and 2.6 times respectively, and the increased amplitudes were significant greater than the effect noted after lidocaine or propranolol treatment. There results suggest that the mechanism of epinephrine-induced cardiac arrhythmias during halothane anesthesia is mainly mediated via alpha-1 receptor and calcium channel, and alpha-1 blocker and calcium channel blocker may be useful to prevent the epinephrine-induced cardiac arrhythmias during halothane anesthesia.
