Myocardial O2 supply and consumption in early cardiac hypertrophy of renal hypertensive rabbits.

This study examined myocardial O2 supply and O2 consumption in hypertension-induced myocardial hypertrophy. New Zealand white rabbits prepared as uninephrectomized (sham) controls (n = 7), or one kidney/one clip (1K1C) hypertensive rabbits (n = 7) were examined four weeks after surgery. A group of renally intact "true" controls (n = 4) was also examined. Coronary blood flow (CBF) was measured with radioactive microspheres in anesthetized open chest animals during baseline and vasodilated conditions (adenosine, 0.4 mg/kg/min). Microvascular O2 saturations were determined by microspectrophotometry. Myocardial oxygen consumption (MVO2) was calculated. Mean pressure was elevated in hypertensive animals (121 +/- 7 mmHg, means +/- SE) compared to uninephrectomized controls (74 +/- 7 mmHg). Hypertrophy was indicated by a 30% increase in heart weight to body weight ratio in the 1K1C animals. The average MVO2 was elevated in hypertrophy (12.4 +/- 0.9 vs. 9.6 +/- 0.8 ml O2/min/100 g). Baseline CBF was higher in cardiac hypertrophy (227 +/- 21 ml/min/100 g) compared to sham controls (169 +/- 14 ml/min/100 g). In hypertrophy the percent increase in CBF during adenosine infusion was reduced and the minimal vascular resistance was higher. No difference in microvascular O2 saturations was observed between groups, thus O2 extraction was similar. No subepicardial vs. subendocardial difference occurred within either the sham controls or the 1K1C animals in any parameter. Therefore, an overall increased MVO2 resulted in increased CBF and reduced coronary flow reserve in short-term renovascular hypertension-induced cardiac hypertrophy in rabbits.