Effect of regression of cardiac hypertrophy on ischemic myocardial damage in spontaneously hypertensive rats.

Effects of reduction of blood pressure and regression of left ventricular hypertrophy following hydralazine and captopril therapy on ischemic cardiac function and myocardial metabolism were studied in spontaneously hypertensive rats (SHR). Hydralazine (1.5 or 3 mg/kg/day) and captopril (50 or 100 mg/kg/day) were administered to SHR from 19 to 26 weeks of age. Both hydralazine and captopril significantly decreased arterial blood pressure in SHR, but only captopril significantly reduced left ventricular weight. The percentage of V3 myosin isozyme significantly decreased in captopril-treated SHR compared to hydralazine-treated SHR. At the end of long-term treatment, hearts were removed and perfused for 15 min by the working heart technique, and then global ischemia was induced for 30 min. The ischemic heart was reperfused for 30 min. In hydralazine-treated SHR and captopril-treated SHR, the pressure-rate product and extent of recovery of the coronary flow during reperfusion following 30 min of ischemia were higher than those in control SHR, but this difference was significant only in captopril-treated SHR. Hydralazine and captopril treatment improved the restoration of the levels of ATP, creatine phosphate, total adenine nucleotide and energy charge potential in SHR after reperfusion following 30 min of ischemia, but only captopril had a significant effect. In conclusion, regression of left ventricular hypertrophy is more important than lowering of blood pressure in order to improve the ischemic myocardial damage.