[Buffering capacity of histidine in cardioplegia analyzed by myocardial production of lactate and alanine].

The buffering capacity of histidine in cardioplegia was analyzed from a viewpoint of anaerobic glycolysis and its end-products (lactate and alanine) by the myocardium. Isolated rabbit hearts were subjected to 3 hours multidose cardioplegic arrest by histidine (195 mM)-buffered or control solution at 21 degrees C and 30 minutes reperfusion. Diastolic pressure (DP) and recovery of developed pressure (DevP%) were measured with an intracavitary balloon filled to a pre-ischemic DP of 8-10 mmHg. Lactate and alanine in tissue and effluent were measured after ischemia by HPLC. The buffered solution group showed lower DP and higher DevP%, production of more lactate and alanine with diffusion of larger part of them into effluent than control group. We conclude that histidine in cardioplegia stimulates production of anaerobic glycolysis-derived high energy phosphate-compounds not only by proton buffering but also by removal of detrimental end-products out of the cell.