Hypothermic cardioplegic arrest is associated with increased myocardial adenosine.

The current study examined the effects of temperature on myocardial pH, contractile function and adenosine triphosphate metabolism, particularly the production of adenosine. We matched intermittent delivery of blood cardioplegia in two groups (hypothermia 15 degrees C; normothermia 37 degrees C), for 2 h of cardioplegic arrest. Hypothermic perfusion resulted in a markedly alkalotic pH, and nearly a threefold increase in adenosine and adenosine monophosphate levels compared to normothermic hearts. Tissue levels of adenosine triphosphate were preserved to the same extent in each group, despite the increased energy requirements of normothermia. Myocardial contractile function was not statistically different between the two groups at 30 min and 2 h after the cross clamp was removed. These data suggest that both methods, hypothermia via its reduced energy demands, and normothermia through continued glycolytic metabolic activity, allow the myocardium to maintain energy stores and resume adequate function. However, hypothermic perfusion results in an accumulation of adenosine, demonstrating that temperature should be considered when attempting to manipulate the generation and accumulation of the compound.