Purine-enriched asanguineous cardioplegia retards adenosine triphosphate degradation during ischemia and improves postischemic ventricular function.

Myocardial dysfunction after induced ischemic arrest is an important problem in cardiac surgery. Adenosine-5'-triphosphate content in myocardial tissue remains depressed for days after ischemia, perhaps because of reperfusion washout of diffusable purine substrates. Left ventricular function is also depressed after ischemia, but its relationship to absolute tissue adenosine triphosphate content is unclear. We tested the hypothesis that arresting hearts with a cardioplegic solution containing adenosine, hypoxanthine, and ribose would result in improved tissue adenosine triphosphate content and left ventricular function after 1 hour of normothermic global ischemia in dogs supported by cardiopulmonary bypass. Animals with ischemic arrest initiated with a crystalloid cardioplegic solution containing adenosine 100 mumol/L, hypoxanthine 100 mumol/L, and ribose 2 mmol/L demonstrated significant improvement (p less than 0.05) during postischemic reperfusion. A significant correlation (p less than 0.05) existed between myocardial adenosine triphosphate content and the recovery of left ventricular function. These experiments demonstrate that an asanguineous cardioplegic solution containing adenosine, hypoxanthine, and ribose maintains myocardial adenosine triphosphate content during ischemia and reperfusion and enhances functional recovery during the postischemic period.