To the Editor:—
We read with interest the article by Gamperl et al. , 1which describes studies evaluating effects of isoflurane on isolated porcine coronary microvessels. The main finding from this well-performed study was that isoflurane caused dilation, which confirmed our results in a similar model. 2
The data from Gamperl et al. 1add to the existing body of compelling evidence that isoflurane is a dilator in the coronary circulation and not a constrictor, as was previously argued. 3We hope that these findings will finally put to rest the controversy relating to the vasomotor effect of isoflurane in the coronary circulation.
Over the past decade, studies in our laboratory 2,4–10and others 1,11,12have sought to clarify the effects of the volatile anesthetics in the coronary circulation. From these studies, several definitive findings have emerged. First, the volatile anesthetics, as a class of drugs, are dose-dependent coronary vasodilators. 1,2,4,6,7,10,11The coronary vasodilating effect of isoflurane is, by far, greater than that of the other volatile anesthetics (halothane, enflurane, sevoflurane, and desflurane). Second, volatile anesthetic–induced coronary vasodilation is mediated by the adenosine triphosphate–sensitive potassium channels 1,2,9,10,12and is endothelium dependent, 1although nitric oxide does not appear to be involved. 5Third, coronary vascular smooth muscle adapts to the relaxing effect of volatile anesthetics 2,5,8; thus, the coronary vasodilation caused by these anesthetics is minimized by slow or extended administrations.
It is worth recognizing that these findings in the coronary circulation served as a springboard for studies demonstrating that the volatile anesthetics may precondition the myocardium against reperfusion injury, 13an action that may have enormous therapeutic value in patients undergoing surgical and nonsurgical coronary revascularization procedures.
