Regression of Cardiac Hypertrophy Normalizes Glucose Metabolism and Left Ventricular Function During Reperfusion

• Published in: Journal of molecular and cellular cardiology 1997-03, Vol.29 (3), p.939-948
• Main Authors: Wambolt, Richard B., Henning, Sarah L., English, Dean R., Bondy, Gregory P., Allard, Michael F.
• Format: Article
• Language: English
• Subjects: Angiotensin-converting enzyme inhibition; Angiotensin-Converting Enzyme Inhibitors - pharmacology; Animals; Blood Pressure; Body Weight; Enalapril - pharmacology; Enalapril maleate; Glucose - metabolism; Glycolysis; Hypertrophy; Hypertrophy, Left Ventricular - metabolism; Hypertrophy, Left Ventricular - pathology; Ischemia; Male; Myocardial Ischemia; Myocardial Reperfusion; Myocardium - metabolism; Myocardium - pathology; Organ Size; Oxidation-Reduction; Peptidyl-Dipeptidase A - blood; Rats; Rats, Sprague-Dawley; Regression; Reperfusion; Ventricular Function, Left
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1006/jmcc.1996.0336

It is not yet known if the alterations in myocardial glucose metabolism and the exaggerated left ventricular dysfunction that occur during reperfusion in hypertrophied hearts are reversible. Thus, we studied isolated working hearts from aortic-banded (n=29) and sham-operated control (n=32) male Sprague–Dawley rats with or without enalapril maleate treatment (25.6±0.8 mg/kg per day, p.o.) to determine the effect of regression of cardiac hypertrophy on myocardial glucose metabolism and post-ischemic heart function. Hearts were perfused with buffer containing 1.2 mmpalmitate, 11 mm[5-3H]/[U-14C]-glucose, 0.5 mmlactate and 100μU/ml insulin. Glucose metabolism [rates of glycolysis (3H2O production) and rates of oxidation (14CO2production) of exogenous glucose] and heart function (heart rate×peak systolic pressure) were measured during 30 min pre-ischemic perfusion and 60 min of reperfusion following 20 min of global, no-flow ischemia. Hearts from untreated aortic-banded rats were hypertrophied, being 27.6±1.8% larger than hearts from untreated control rats. Enalapril treatment caused regression of cardiac hypertrophy that normalized heart weight in aortic-banded rats. Rates of glycolysis of exogenous glucose in hearts from untreated aortic-banded rats were accelerated compared to rates in hearts from untreated control rats during pre-ischemic perfusion (4391±97v2652±69 nmol glucose/min per g dry wt, respectively,P