The Antiarrhythmic Effect of MgSO4 pretreatment in CaCl2-Caused Increase in Epinephrine Induced Ventricular Arrythmia.
10.4097/kjae.1994.27.8.867
- Author:
Jung Won PARK
1
;
Mi Kyoung LEE
;
Nan Sook KIM
Author Information
1. Department of Anesthesiology, College of Medicine, Korea University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Magnesium;
Calcium;
Epinephrine-induced-arrhythmia
- MeSH:
Alcoholism;
Anesthesia;
Arrhythmias, Cardiac*;
Calcium;
Calcium Channel Blockers;
Coronary Artery Disease;
Digitalis;
Epinephrine*;
Halothane;
Magnesium;
Myocardial Ischemia;
Poisoning;
Potassium;
Rabbits;
Salts;
Sodium
- From:Korean Journal of Anesthesiology
1994;27(8):867-873
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Magnesium salts have been reported to be effective in the treatment of atrial, junctional and ventricular arrhythmias resulting from myocardial ischemia, digitalis poisoning, alcoholism, diuretic therapy and coronary artery disease. The mechanism of antiarrhythmic effect is thought to inhibit the efflux of potassium, supress inward sodium movement, and mimic calcium channel blocking drugs by inhibiting cellular calcium uptake. The purpose of this study is to evaluate the antiarrhythmic effect of MgSO4 by inhibiting intracellular calcium transport and dose-related effect. The experiments were composed of four steps. 16 ug/Kg of epinephrine was injected in twenty rabbits anesthetized with halothane (experiment 1). Ventricular arrhythmia was developed in all rabbits. At 15 minutes later, after the retum of sinus rhythm, CaCl2 (10 mg/Kg) was injected slowly for 5 min, and than 16 ug/Kg of epinephrine was injected immediately after the administration of CaC12 (experiment 2). After 45 mins, 8 mg/Kg (experiment 3, n=10) and 16 mg/Kg (experiment 4, n=10) of MgSO4 were injected for 5 mins, and than CaCl2 and epinephrine were administrated as experiment 2. The onset and duration of ventricular arrhythmia following each experiment were observed. The results were as follows; 1) 16 ug/Kg of epinephrine induced ventricular arrhythmia in all cases. 2) CaCl2 infusion caused a reduction in onset and increase in duration of epinephrine-induced-arrhythmia, but there was no significanee. 3) MgSO4-pretreatment caused a increase in onset and reduetion in the CaCl2-caused increase in arrhythmia duration. Only MgSO4-16 mg/Kg values were significant. In conclusion, magnesium salts pretreatment demonstrated effectiveness in preventing ventricular arrhythmia associated with epinephrine usage and hypercalcemic condition during halothane anesthesia.
