TEMPERATURE THRESHOLD AND MODULATION OF ENERGY-METABOLISM IN THE CARDIOPLEGIC ARRESTED RABBIT HEART

Hypothermia protects ischemic tissues by reducing ATP utilization and accumulation of harmful metabolites. However, it also reduces ATP prod uction, which might cause deterioration in the energy supply/demand ra tio. Modulation of energy supply/demand according to temperature has n ot been previously studied in detail. In this study, isolated, perfuse d rabbit hearts (n = 60) were used to determine the effects of various temperatures on myocardial energy metabolism and function during card ioplegic arrest. Ischemia was induced by crystalloid cardioplegic solu tion at 4, 18, 30, and 34 degrees C for 120 min, respectively. At each temperature, the hearts were divided into a glucose-treated group whi ch contained 22 mM glucose in cardioplegic solution as the only substr ate and a control group which contained 22 mM mannitol to keep same os molarity. Following 15 min reperfusion, recovery of left ventricular d eveloped pressure (DP), +/- dP/dt(max), and the product of heart rate and DP were significantly higher in 30, 18, and 4 degrees C groups tha n those in 34 degrees C control group. The functional recovery was als o significantly higher in the 34 degrees C glucose-treated group than that in the 34 degrees C control group, but there was no difference be tween these groups at 30 degrees C and the temperature below 30 degree s C. Myocardial ATP concentration was significantly lower in 34 degree s C control group than those in other groups. There is a close relatio nship between myocardial ATP concentration and functional recovery (R- 2 = 0.90). The accumulations of lactate and CO2 were significantly hig her at 34 degrees C in glucose-treated group than those in the control group. However, there was no significant difference between these two groups at 30 degrees C and the temperature below 30 degrees C. These results indicate that under these study conditions: (1) a marked decre ase in energy supply/demand occurs above 30 degrees C, implying that a temperature threshold exists; and (2) this can be ameliorated by prov ision of glucose as substrate in cardioplegia solution. (C) 1998 Acade mic Press.