Coronary autoregulation

Abstract

Autoregulation of coronary blood flow is complicated because the heart provides the blood flow and pressure for its own perfusion. Aortic pressure is not only the perfusion pressure for the coronary circulation, but is also the afterload for the left ventricle. Coronary autoregulation has therefore been studied when the coronary circulation is cannulated and perfused separately from the aorta. Even then, changes in coronary artery pressure result in alterations in myocardial metabolism due to the Gregg effect. Local metabolic vascular control appears to be the dominant factor in coronary autoregulation. If myocardial metabolism is enhanced, coronary autoregulation occurs at a higher level of flow. The balance between myocardial oxygen supply and demand is critical for coronary autoregulation, since good autoregulation is only observed when the coronary venous oxygen tension is near the normal value of about 20 mmHg. At present there is little evidence for a myogenic mechanism of coronary autoregulation, and adenosine also does not seem to be involved. It is concluded that coronary autoregulation is predominantly due to a local metabolic mechanism, but the substance that mediates the control is unknown.