Effects of hypoxia and ischaemia on coronary vascular resistance, A-V node conduction and S-A node excitation.

Hypoxia and ischaemia produce relaxation of the vascular smooth muscle of the resistance vessels in the myocardium. A low pH may contribute to the arteriolar dilatation but cannot account for the major response. In all likelihood the reduced pO2 acts indirectly by release of a vasodilator mediator rather than by a direct effect on the vascular muscle. Potassium release may account for a transient component of the vasodilation, but it appears that a major factor is the release of adenosine from the ischaemic tissue. Adenosine also appears to be responsible for slowing of the sinus rate and impaired A-V conduction in myocardial ischaemia. These observations are of clinical significance because hypoxia-induced A-V block, such as may occur in inferior myocardial infarction, can be abolished by an adenosine antagonist such as aminophylline. In contrast, adenosine is also useful in the treatment of some cardiac arrhythmias. Supraventricular tachycardia, in which the A-V node is involved in the re-entrant pathway, is readily abolished in humans by the intravenous administration of small doses of adenosine.