INTRACORONARY ISOFLURANE CAUSES MARKED VASODILATION IN CANINE HEARTS

Previous studies of coronary vasomotor effects of isoflurane were complicated by changes in systemic hemodynamic conditions and in global cardiac work demands. Accordingly, in the current study, the left anterior descending coronary artery (LAD) of 11 open-chest dogs anesthetized with fentanyl and pentobarbital was cannulated and perfused with isolfurane-free arterial blood or with arterial blood equilibrated in an extracorporeal oxygenator with isoflurane (0.5, 1.0, 2.0% in 95.5% oxygen-4.5% carbon dioxide). Steady-state changes in coronary blood flow (CBF) in LAD were measured electromagnetically, and their transmural distribution (endocardium: epicardium ratio) was evaluated with 15-mu-m radioactive microspheres. Venous blood was obtained from the anterior interventricular vein and analyzed for oxygen tension (P(o2)) and oxygen content. Myocardial oxygen consumption (MV(o2)) was calculated using the Fick equation. Cardiac responses during isoflurane were compared to those during maximal vasodilation with intracoronary adenosine. Perfusion pressure was maintained at 100 mmHg. CBF increased 271, 279, and 503% with 0.5, 1.0, and 2.0% isoflurane, respectively, with no change in the endocardium:epicardium ratio. With 2.0% isoflurane, the increase in CBF was 80% of the maximal, adenosine-induced response. The increases in CBF caused by isoflurane were accompanied by greater than proportional increases in venous P(o2) and decreases in the arteriovenous oxygen difference, reflecting the reduction (approximately 40%) in MV(o2)). In conclusion, isoflurane has a direct, concentration-dependent relaxing effect on coronary vascular smooth muscle in the canine heart in situ. The ability of isoflurane to increase CBF nearly maximally while also significantly reducing local myocardial oxygen requirements attests to the potency of isoflurane's direct vasodilator action.