Effects of intracoronary infusion of adenosine on cumulative deterioration of regional myocardial wall motion induced by repeated brief periods of coronary occlusion in anesthetized dogs.

The present study was performed to evaluate the effects of the intracoronary infusion of adenosine on regional wall motion in the canine heart subjected to repeated brief coronary occlusion and reperfusion. In anesthetized open-chest dogs, six episodes of five-minute coronary occlusion followed by a fifteen-minute reperfusion were performed. Animals received infusions of either adenosine or saline (control) into the coronary artery during the initial five minutes of each reperfusion. Changes in regional wall motion were studied by means of ultrasonic crystals. The authors prolonged the duration of hyperemic flow at each reperfusion in a third group by means of a roller pump to examine whether the increase in coronary flow during reperfusion itself might affect the process of the deterioration of regional wall motion. In the control dogs, wall thickening decreased progressively after each reperfusion. However, in the adenosine-treated animals, regional wall motion fifteen minutes after the sixth reperfusion did not differ from baseline. Prolongation of hyperemic flow did not improve the progressive decline in regional wall motion. Thus, adenosine prevented the cumulative decrease in the regional wall motion of the myocardium treated with a series of repeated transient coronary occlusions, most likely by a mechanism unrelated to its vasodilating action.

Coronary pressure-flow, pressure-function, and function-myocardial oxygen consumption relations in postischaemic myocardium.

STUDY OBJECTIVE: The aim was to study coronary pressure-flow, pressure-myocardial wall motion and myocardial wall motion-myocardial oxygen consumption relations in postischaemic myocardium with prolonged myocardial dysfunction (stunned myocardium) in comparison with normal myocardium. DESIGN: Regional myocardial wall thickening was measured with ultrasonic crystals, and postischaemic myocardial dysfunction was achieved by occlusion of a carotid-left anterior descending coronary artery bypass (15 min) and reperfusion (30 min). Coronary perfusion pressure was decreased in 10 mm Hg steps by constricting the bypass before and after producing postischaemic myocardial dysfunction. At each constriction step, coronary flow, regional wall thickening, and regional myocardial oxygen consumption in the area perfused by the left anterior descending artery were measured. EXPERIMENTAL MATERIAL: 12 anaesthetised open chest mongrel dogs, weighing 12-16 kg, were studied. MEASUREMENTS AND MAIN RESULTS: At the basal level, myocardial wall thickening of postischaemic myocardium was depressed compared to normal myocardium, at 18.5(SD 8.9)% v 1.3(7.1)%, p less than 0.01. With coronary stenosis, wall thickening gradually decreased at a coronary pressure below 60 mm Hg in normal myocardium, but remained unchanged until mean coronary pressure was reduced to 50 mm Hg in postischaemic myocardium. Myocardial wall thickening of postischaemic myocardium was always more depressed than normal myocardium. At any level of coronary pressure, coronary flow in postischaemic myocardium was not different from normal myocardium. There was no difference in regional myocardial oxygen consumption between normal and postischaemic myocardium at any level of coronary pressure. However, regional myocardial oxygen consumption in postischaemic myocardium was higher than in normal myocardium performing similar levels of myocardial wall thickening. CONCLUSION: The coronary pressure-function relation but not the pressure-flow relation changed in postischaemic myocardium after a 15 min coronary occlusion. Regional myocardial oxygen consumption was relatively increased in postischaemic myocardium.