Effect of anesthesia on reactivity of large coronary arteries in the dog

Epicardial coronary arteries dilate after release of a transient coronary occlusion in awake chronically instrumented dogs but not in anesthetized dogs studied acutely after surgery. To determine whether anesthesia or surgical trauma is responsible for this lack of reactive dilation, we evaluated the effect of anesthesia on reactive coronary dilation in six chronically instrumented dogs. Circumflex coronary diameter was measured with sonomicrometry. Response to release of a 20- or 30-s coronary occlusion was studied before and after sodium pentobarbital (20 ± 2 mg/kg) and before and after α-chloralose (100 mg/kg) plus either morphine or fentanyl and droperidol. Pentobarbital blunted the peak flow response to release of a transient coronary occlusion (114 ± 15 vs. 128 ± 16 ml/min, p < 0.05) but did not affect the increase in large coronary diameter (before pentobarbital: 3.68 ± 0.30-3.74 ± 0.30 mm; after pentobarbital: 3.66 ± 0.31-3.71 ± 0.31 mm). α-Chloralose blunted the peak flow response to release of a transient coronary occlusion (96 ± 12 vs. 141 ± 25 ml/min, p < 0.05) but did not affect the increase in large coronary diameter (before chloralose: 4.00 ± 0.28-4.06 ± 0.28 mm; after chloralose: 3.91 ± 0.31-3.98 ± 0.31 mm). Therefore, each drug blunted the peak flow response to release of a transient coronary occlusion, but dilation of large coronary arteries was not impaired. The lack of reactivity of large coronary arteries in acutely studied dogs is probably due to the trauma of recent surgery and not the anesthesia.