Coronary endothelium-derived vasodilation during cooling and rewarming of the in situ heart

The integrity of coronary vascular endothelial vasodilator function during core cooling and rewarming was investigated in a pentobarbital-anesthetized open-chest dog model. Vasodilator response was assessed as the change from baseline blood flow by injecting the endothelial-dependent vasodilator ace tylcholine (ACh) (1.0 mu g) or the endothelial-independent vasodilator nitr oglycerin (NTG) (50 mu g) into the left anterior descending (LAD) coronary artery. Change in blood flow was measured using a transit time ultrasonic v olume flowmeter technique. During cooling and rewarming LAD blood flow was significantly decreased. After rewarming, aortic pressure was artificially elevated to reach control. This procedure restored heart work (LV-RPP, left ventricular rate pressure product) and coronary perfusion pressure, but LA D blood flow remained lowered. Ability to dilate the vascular bed supplied by LAD, after injections of ACh or NTG, was present both during cooling and rewarming. At 25 degrees C coronary blood flow (LAD) increased from 3 +/- 1 to 9 +/- 1 mL.min(-1) in response to both ACh and NTG. Posthypothermic bl ood flow increased from 7 +/- 1 to 19 +/- 2 and 20 +/- 3 mL.min(-1) in resp onse to ACh and NTG, respectively. Measured as the percent change from base line LAD blood flow, the response was not significantly different from the one obtained in prehypothermic hearts. In conclusion, coronary vasodilator function, both endothelium dependent and endothelium independent, is presen t but not maintained at the same level during cooling to 25 degrees C and r ewarming. In spite of the deterioration of cardiac function, no selective d efect in the endothelium-dependent response was detected, either during hyp othermia or after rewarming.