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A B S T R A C T This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = ±9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K+, but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na+.There was no detectable release of adenosine by hearts during pacing or exercise in three control groups of patients: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure.The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.A preliminary abstract of this work appeared in: 1971. Circulation. 44(Suppl. II): 65.

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By means of right and left heart catheterization 70 patients with congenital or acquired heart disease were examined to determine whether or not a gradient in pressure existed between the pulmonary artery and the left ventricle at the end of diastole. In the absence of mitral valvular obstruction in 56 patients there was a statistically significant correlation of pulmonary artery diastolic, left ventricular end-diastolic, and left atrial mean pressures less than 15 mm Hg which was independent of heart rate. Diastolic pressures at identical levels as high as 40 mm Hg were demonstrated in the presence of aortic insufficiency without left ventricular failure, and as high as 47 mm Hg during pulmonary edema in one patient with aortic stenosis and insufficiency. A diastolic gradient in pressure between the pulmonary artery and the left ventricle existed in 14 patients with pulmonary hypertension. These patients all had congenital intracardiac shunts and it may be assumed that they had some obstruction in the pulmonary vascular bed. These findings suggest that within defined limits friction across the pulmonary vascular bed is so small that a state of pressure equilibrium exists at the end of diastole. When the limits are met clinically, the pressures in the pulmonary artery and in the left ventricle at the end of diastole are identical.