Isoproterenol and myocardial O2 supply/consumption in hypertension-induced myocardial hypertrophy.

Myocardial oxygen supply, O2 consumption (MVO2) and function were determined during base-line and isoproterenol infusion (0.5 microgram.kg-1.min-1) 30 days after New Zealand White rabbits were prepared as one-kidney, one-clip (1K,1C) Goldblatt hypertensive or uninephrectomized (sham) controls. Coronary blood flow and cardiac output, using radioactive microspheres, and small vessel O2 saturations, using microspectrophotometry, were measured in hypertrophied and nonhypertrophied hearts. After 30 days, 33% myocardial hypertrophy was evident in the 1K,1C animals. Base-line blood pressure was significantly higher in the 1K,1C animals compared with sham controls and remained higher during isoproterenol infusion. Base-line heart rate was not different between animal groups, and heart rate increased in both groups during isoproterenol. Cardiac output was similar between sham and 1K,1C animals during base-line conditions (316 +/- 40 vs. 365 +/- 51 ml/min, respectively). After isoproterenol, cardiac output increased in the sham animals (494 +/- 119 ml/min) but not in the 1K,1C group (317 +/- 85 ml/min). Isoproterenol elevated MVO2 threefold in both the sham and 1K,1C animals. Coronary blood flow was significantly increased to similar levels in both animal groups. O2 extraction significantly increased during isoproterenol in both groups. Therefore, impaired cardiac function was evident during isoproterenol stress in the hypertrophied myocardium independent of myocardial O2 supply or consumption restrictions.