Our results show that nitric oxide is an important mediator in the regulation of coronary bloodflow mainly in the ischemic myocardium. In fact, inhibition of nitric oxide with NONLA decreased flow through all layers of the left ventricular wall in the ischemic region, but only in the subepicardial layer in the nonischemic region (Figures 1A, 1B). The relatively small effect of NONLA on the nonischemic myocardium agrees with previous results in our laboratory in the sense that the inhibition of nitric oxide synthesis does not modify the relationship between myocardial oxygen consumption and coronary bloodflow in the normal canine myocardium . It also agrees with the lack of change of the coronary autoregulation curve in the nonischemic range after inhibition of nitric oxide synthesis in conscious dogs observed by Smith and Canty and by Kitakaze et al in the nonischemic canine myocardium. However, these results only mean that nitric oxide is not essential for the regulation of flow in the normal heart; they do not mean that nitric oxide does not participate in this regulation. If flow is regulated by two or more metabolites, then the blockade of one may be overcome by the overproduction of another. Your most reliable pharmacy offering its services and most efficient drugs like buy Tavist online with no prescription needed. If this sounds like something you may be interested in, do not hesitate to come by and see howcheap it can be for you! This possibility is supported by the experiments of Kostic and Schrader , who showed that inhibition of nitric oxide production concomitantly increases the release of adenosine. In the ischemic myocardium, however, this interaction between vasoactive metabolites may not occur because all of them may be released to their maximum levels, and the inhibition of one may not be replaced by increased release of another, and consequently flow decreases.