Myocardial ischemia in human hypertension and in various animal models of hypertension may be due to abnormal maximal coronary vasodilator reserve and disturbaces of coronary vasomotion. The vascular reactivity defects in hypertension have been associated with the defective endothelium and sympathetic neural activation. However, such abnormalities in hypertension need to be elucidated. In the present study the effectsof cardiac ischemia reperfusion on coronary circulation, intramyocytic adenylates and purine nucleosides were examined in Langendorff-perfused Sprague Dawley rat (SD) and spontaneously hypertensive rat (SHR) hearts. Coronary venous and cardiac lactate and cardiac pyruvate were also measured. It should be noted that in the regulation of coronary flow the intrinsic flow autoregulation is highly variable due to coexisting metabolic flow control, and that natural coronary flow and cardiomyocytic energy state are normally reciprocally related in perfused heart.

For the Langendorff heart perfusion, bicarbonate perfusion buffer (pH 7.40±0.02,37℃) was equilibrated with 95% O₂ : 5% CO₂ and contained 5mM glucose (+5U/1 insulin) and 2mM pyruvate as energy-yielding substrates. Global hypoperfusion ischemia was induced by lowering coronary perfusion pressure of 100 to 40 cmH₂O, followed by 20 min reperfusion.

During the ischemia and reperfusion, metabolic acidosis and enhanced venous lactate output in SHR were observed with increases in coronary vascular resistance and myocardial oxygen consumption.In addition, coronary reactive hyperemia during reperfusion was depressed. Although ischemia-induced increase in combined adenosine plus inosine were abolished during prolonged reperfusion, SD still exhibited coronary vasodilation. The depressed reactive hyperemia in SHR was associated with decreases in cardiac adenosine triphosphate (ATP) pool and creatine phosphate/inorganic phosphate (CrP/Pi) ratio and an increase in cardiac lactate/pyruvate ratio.

This abnormal vascular reactivity during ischemia and reperfusion in SHR may be in part due to an alteration in the cardiac energy state and hence to a mismatch between myocardial metabolic demand and supply.