[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.
Ohkado
A
A
Department of Cardiothoracic Surgery, University of Pittsburgh School of Medicine.
Cao-Danh
H
H
Sommers
K E
KE
del Nido
P J
PJ
D000409:Alanine / Q000096:biosynthesis*; D000693:Anaerobiosis; D000818:Animals; D002021:Buffers; D002314:Cardioplegic Solutions; D006324:Heart Arrest, Induced; D006639:Histidine / Q000494:pharmacology*; D066298:In Vitro Techniques; D007773:Lactates / Q000096:biosynthesis*; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism*; D011817:Rabbits
D002021:Buffers; D002314:Cardioplegic Solutions; D007773:Lactates; D019344:Lactic Acid; D006639:Histidine; D000409:Alanine