Influence of vasodilators upon function and metabolism of ischemic myocardium

Although the systemic hemodynamic effects of vasodilators such as nitroprusside, phentolamine and nitrates are well known, relatively little information is available regarding their effects upon the function and metabolism of ischemic myocardium. Experimental and clinical studies indicate that vasodilators improve the mechanical performance of regional ischemic myocardium, probably by simultaneous reduction of peripheral resistance and reduction of the degree of ischemia. The majority of evidence, although still controversial, seems to indicate that myocardial perfusion can also be increased, particularly when coronary collateral vessels are present. Concomitant reduction in preload contributes to reduced oxygen demand, as evidenced by findings of reduced oxygen extraction. Thus, the balance of the oxygen supply and demand may be improved as indicated by decreases in lactate production. In addition, limited evidence in experimental animals and man suggests that vasodilators may also reduce the extent of myocardial injury as measured by S-T segment mapping and the creatine phosphokinase (CPK) release technique. However, these effects are contingent upon the arterial pressure response, and directionally opposite results may be anticipated if hypotension occurs. Since the mechanism of action of vasodilators is reasonably well understood, vasodilator therapy can be administered safely in anticipation of both improvement in total cardiac performance and a decrease in severity of ischemia.