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

Summary

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 mm Hg,$\bar X \pm SE$) compared to uninephrectomized controls (74±7 mm Hg). 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.