Myocardial high-energy phosphate replenishment during ischemic arrest: aerobic versus anaerobic metabolism

An in vivo, isolated pig heart preparation was used to study the effect of L-glutamate added to crystalloid and blood potassium cardioplegia on the myocardial high-energy phosphate compounds, adenosine triphosphate (ATP) and creatine phosphate (CP). Studies were performed during a three-hour arrest interval and during 60 minutes of reperfusion. Levels of ATP remained at or above control levels during arrest in animals receiving either unmodified blood or glutamate-enriched crystalloid cardioplegia. While glutamate significantly improved the ability of the crystalloid solution to preserve ATP during arrest, when added to blood, it contributed to a depressed ATP after a three-hour arrest. Creatine phosphate declined during arrest in all animals, but those receiving unenriched blood cardioplegia consistently had the highest levels (p less than 0.05). Addition of glutamate to crystalloid cardioplegia provided a significantly (p less than 0.05) higher level of CP at the end of three hours of arrest, which was still lower than that noted with unenriched blood. Comparable to its effect on the ATP level, when glutamate was added to blood cardioplegia, a decrease (p less than 0.05) in CP was noted after three hours of arrest. Attempts to enhance high-energy phosphate production by supplementing blood cardioplegia with L-glutamate are ineffective, while increased high-energy phosphate production results when glutamate is added to crystalloid cardioplegia. This implies that L-glutamate functions where anaerobic and not aerobic metabolism is the major component of preservation. With reperfusion, the only group of animals displaying depressed levels of ATP and CP was that receiving glutamate-enriched blood cardioplegia.