Lack of effect of nitroglycerin on the transmural variation of tissue pH during fixed coronary stenosis

A new MpH-measuring system was used to investigate the mechanism of action of intravenous NTG on pacing-induced myocardial ischemia during critical stenosis. In ten anesthetized open-chest dogs, two MpH electrodes were placed in a segment supplied by the CCA, one superficial and one deep. Atrial pacing at a rate 50 beats/min higher than baseline was instituted for a period of 10 min (Pacing I). Critical stenosis was then applied to the CCA. Three more similar periods of atrial pacing were instituted during critical stenosis. Pacing II was without any intervention, Pacing III was after the intravenous administration of a bolus of NTG, and Pacing IV was after the intravenous administration of NTG + A. NTG (metamarinol) during critical stenosis and atrial pacing did not alter preload and did not reduce afterload more than critical stenosis and atrial pacing alone. It did not significantly alter flow in the CCA measured by an electromagnetic flow meter. Consequently, the magnitude of fall in both endo- and epicardial MpH during critical stenosis and atrial pacing was no different with or without the administration of NTG. That under these conditions NTG failed to reduce the degree of myocardial ischemia suggests that the beneficial effects of NTG during fixed critical stenosis are determined primarily by its ability to reduce the determinants of myocardial oxygen demand, and not by a direct effect on the ischemic myocardium per se. The study also demonstrates for the first time a significant transmural gradient in MpH in the canine heart, even in the normal resting state.