Glutamate-blood cardioplegia improves ATP preservation in human myocardium.
Two groups of patients subjected to radical correction of Fallot's tetrad and defects of interventricular septum were investigated to ascertain whether the addition of glutamic acid to blood cardioplegic perfusate could improve preservation of myocardial ATP during cardiac arrest. In the control group (17 patients) the myocardial protection was performed by repeated infusions of cold blood potassium cardioplegic solution; in the 2nd group (24 patients) cardioplegic perfusate containing glutamic acid (20 mmol/l) was used. Left ventricular biopsies were taken during the first minute after cross-clamping of the aorta and before the release of the aortic clamp to determine ATP, glutamate and lactate. The cross-clamping time averaged 32 min in both groups. In the patients of the control group the losses of ATP correlated with the decrease in glutamate during the clamping period. A maintenance of a higher myocardial glutamate content by glutamate-containing cardioplegic perfusate prevented ATP fall or increased its level in patients of the 2nd group. There was no significant difference in lactate levels between the two groups by the end of the cardiac arrest. We conclude that enrichment of blood cardioplegic solution by glutamic acid, which may act as a substrate for anaerobic energy production, provides more effective myocardial protection during ischemic heart arrest.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D001769:Blood; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003326:Coronary Circulation; D005971:Glutamates / Q000378:metabolism / Q000494:pharmacology*; D018698:Glutamic Acid; D006324:Heart Arrest, Induced; D006801:Humans; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism*; D013771:Tetralogy of Fallot / Q000601:surgery
D002314:Cardioplegic Solutions; D005971:Glutamates; D007773:Lactates; D019344:Lactic Acid; D018698:Glutamic Acid; D000255:Adenosine Triphosphate