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.