Coronary distending pressure and delayed myocardial ischemia

The role of blood pressure alterations in the delayed onset of myocardial ischemia following sympathetic stimulation was studied in seven anesthetized dogs. In the presence of coronary stenosis, stimulation of the left stellate ganglion produced significant increases in heart rate and mean aortic pressure, but not in mean coronary blood flow or intracoronary pressure. Following cessation of stimulation, heart rate and aortic pressure returned to control levels over a 1- to 2-minute period. During this time, there was a progressive coronary vasoconstriction, as indicated by a significant fall in coronary arterial flow and intracoronary pressure. When the hypertensive response to stellate stimulation was prevented by controlled exsanguination, the coronary vasoconstriction was not delayed but occurred during stimulation. In the second phase of experiments, the aorta was constricted so as to raise systemic pressure to the peak level achieved during stimulation. Elevation of systemic pressure consistently restored coronary arterial blood flow and intracoronary pressure to the control values. By contrast, induction of hypertension by restimulation of the stellate ganglion failed to reverse the delayed coronary vasoconstriction. We conclude that delayed myocardial ischemia results from the imbalance between coronary distending pressure and an alpha-adrenergically mediated vasoconstrictor activity that persists following cessation of sympathetic nervous system stimulation.