title: Cardioprotective effects of various class I antiarrhythmic drugs in canine hearts.
abstract: This study was designed to clarify the cardioprotective effects of various class I antiarrhythmic drugs, i.e., aprindine, disopyramide, flecainide, lidocaine, mexiletine, pentisomide and propafenone, on the ischemic heart. Sixty-one adult mongrel dogs were classified into eight groups according to premedication: 1) control group, physiologic saline solution was administered intravenously 25 min before left anterior descending coronary artery ligation; 2) aprindine group, 3 mg/kg body weight of aprindine intravenously; 3) disopyramide group, 2 mg/kg of disopyramide intravenously; 4) flecainide group, 2 mg/kg of flecainide intravenously followed by drip infusion of 100 micrograms/kg per min; 5) lidocaine group, 2 mg/kg of lidocaine intravenously followed by drip infusion of 100 micrograms/kg per min; 6) mexiletine group, 3 mg/kg per min of mexiletine intravenously followed by drip infusion of 15 micrograms/kg per min; 7) pentisomide group, 5 mg/kg intravenously; and 8) propafenone group, 2 mg/kg intravenously. Arterial blood pressure and electrocardiogram were monitored throughout the experiment. Two hours after coronary occlusion, the heart was excised. Myocardial mitochondria were prepared and mitochondrial function (the respiratory control index and the rate of oxygen consumption in state III) was measured polarographically. Fractionation of myocardial tissues was performed and the lysosomal enzyme (N-acetyl-beta-glucosaminidase and beta-glucuronidase) activities among fractions were measured. No significant hemodynamic changes were observed compared with the control group except for those in the disopyramide and flecainide groups; that is, decrease in heart rate without changes in blood pressure compared with the control group was observed. All antiarrhythmic drugs effectively prevented the development of ventricular arrhythmias associated with ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, University of Nagoya, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Hanaki
authors.forename: S
authors.initials: S
authors.lastname: Sugiyama
authors.forename: N
authors.initials: N
authors.lastname: Hieda
authors.forename: K
authors.initials: K
authors.lastname: Taki
authors.forename: H
authors.initials: H
authors.lastname: Hayashi
authors.forename: T
authors.initials: T
authors.lastname: Ozawa
mesh_terms: D000118:Acetylglucosaminidase / Q000378:metabolism; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D003327:Coronary Disease / Q000150:complications* / Q000378:metabolism; D004285:Dogs; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D008247:Lysosomes / Q000187:drug effects / Q000201:enzymology; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects
chemical_list: D000889:Anti-Arrhythmia Agents; D000118:Acetylglucosaminidase