Captopril improves recovery of adenosine triphosphate during reperfusion of the ischemic isolated rat heart; a 31-phosphorus-nuclear magnetic resonance study

The effect of captopril on energy-rich phosphates and pH during normothermic ischemic arrest, hypothermic cardioplegic arrest and subsequent reperfusion was investigated in the isolated rat heart using 31P-nuclear magnetic resonance. The hearts remained in the probe during all perfusion procedures and captopril (80 ml·l-1) treatment was started directly after cannulation. After normothermic ischemic arrest (15 min), the ATP content of captopril-treated hearts was not significantly different from that of untreated hearts (53±9% and 52±8%, respectively). Accumulation of inorganic phosphate at the end of ischemia was significantly less in treated hearts, suggesting a higher end-ischemic nucleotide content in treated hearts. Hypothermic cardioplegic arrest (St. Thomas' Hospital solution, 4°C) lasted for 3h at 10°C. Adenosine triphosphate in treated hearts was significantly lower at the end of ischemia; 36±6% compared to 53±9% for untreated hearts. Adenosine triphosphate in untreated hearts recovered to 76±9% after normothermic ischemia and to 72±7% after hypothermic ischemia at the end of 30 min reperfusion. Captopril significantly improved adenosine triphosphate recovery in both treated groups; 89±4% after normothermic and 83±4% hypothermic ischemia. We conclude that captopril has a beneficial effect on recovery of adenosine triphosphate both after normothermic and after hypothermic ischemia.