Regression of left ventricular hypertrophy and susceptibility to reperfusion-induced arrhythmias after DOCA-salt hypertension in the rat.
Treatment with deoxycorticosterone acetate (DOCA) and salt for 12 weeks consistently induced hypertension in rats. Groups of treated rats and age-matched normotensive controls were killed 2 and 14 weeks after stopping the treatment. Two weeks after treatment with the corticoid, all the treated rats had left ventricular hypertrophy. Fourteen weeks after treatment the spontaneous regression of the hypertension was very variable, giving a wide range of ratios of left ventricular to body weight. The hearts were Langendorff-perfused and subjected to occlusion of the left coronary artery for 10 minutes at 37 degrees C. During reperfusion for 5 minutes, the severity of ventricular tachycardia and ventricular fibrillation was assessed. Two weeks after treatment, the incidence and duration of ventricular fibrillation were significantly greater in the treated hearts than in normal hearts. Fourteen weeks after treatment, the hearts with a ratio of left ventricular to body weight greater than 2.40 mg/g displayed a greater incidence of sustained ventricular fibrillation than controls and the median duration of ventricular fibrillation in this group was high. Conversely, the incidence of sustained ventricular fibrillation was lower in the treated group in which regression of the ratio of left ventricular to body weight was less than 2.40 mg/g; and the median duration of ventricular fibrillation was also reduced after regression of the left ventricular hypertrophy. This study provides evidence that regression of left ventricular hypertrophy may confer a reduced susceptibility to arrhythmias.
Baxter
G F
GF
Department of Pharmacology, De Montfort University, Leicester, UK.
Yellon
D M
DM
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D003900:Desoxycorticosterone; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D015425:Myocardial Reperfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D012075:Remission, Spontaneous; D012965:Sodium Chloride; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology
D003900:Desoxycorticosterone; D012965:Sodium Chloride