Benefits of normothermic induction of blood cardioplegia in energy-depleted hearts, with maintenance of arrest by multidose cold blood cardioplegic infusions.
This study tests the hypothesis that warm induction of cardioplegia prior to prolonged maintenance by multidose infusions of cold blood cardioplegic solution would increase the tolerance of energy-depleted hearts to subsequent aortic clamping. Eighty percent depletion of subendocardial adenosine triphosphate (ATP) was produced in 30 dogs by 45 minutes of normothermic ischemia. This was followed either by unmodified blood reperfusion or 2 additional hours of aortic clamping with multidose cold blood cardioplegia. We compared a brief (5 minute) period of 37 degrees C cardioplegic induction to standard 4 degrees C blood cardioplegic induction to determine if warm induction would enhance metabolic and functional recovery. Warm cardioplegic induction resulted in more oxygen consumption than cold induction (16.9 versus 8.1 cc/100 gm), and lower levels of glucose-6-phosphate (G6P), suggesting better aerobic metabolism (0.97 versus 1.87 microM/gm wet weight). Prompt repletion of creatine phosphate (CP) occurred with warm and cold cardioplegic induction, although ATP levels levels remained low. Hearts undergoing ischemia and unmodified reperfusion consumed insufficient oxygen to meet basal metabolic needs during reperfusion (7 cc/100 gm below requirement) and recovered only 33% +/- 5% of control left ventricular performance. Better function occurred with cold cardioplegic induction (63% +/- 5%), and almost complete recovery (85% +/- 5%) occurred when warm induction of cardioplegia was used. We conclude that warm induction followed by prolonged cold multidose blood cardioplegic arrest enhances aerobic metabolism, results in normal left ventricular performance, and improves tolerance of aortic clamping in energy-depleted hearts.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D003327:Coronary Disease / Q000209:etiology; D004285:Dogs; D006324:Heart Arrest, Induced / Q000009:adverse effects / Q000379:methods*; D009206:Myocardium / Q000032:analysis* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010725:Phosphocreatine / Q000032:analysis
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D010100:Oxygen