Metabolic and functional effects of progressive degrees of hypothermia during global ischemia

Recent studies from this laboratory demonstrated that the myocardial protection provided by cooling the heart to 27°C during global ischemia can be improved by the additional use of potassium cardioplegia. The present investigation was designed to determine if further lowering of the myocardial temperature below 27°C could, in itself, result in additional myocardial protection. Feline heart preparations subjected to 60 min of global ischemia and 45 min of normothermic (37°C) reperfusion were divided into four groups: eight maintained at 37°C, 27°C, 20°C, and 10°C. Myocardial carbon dioxide tension, measured by mass spectrometry, during the 60 min ischemic period rose to 342±18 mmHg in 37°C hearts, to 231±11 mmHg in 27°C hearts, to 105±6 mmHg for 20°C hearts, and to 56±4 mmHg for 10°C hearts. In all four groups myocardial oxygen tension fell to comparably low levels (<10 mmHg) during the ischemic period. Myocardial function, as assessed by peak developed ventricular pressure and dP/dtmax, was improved compared to the normothermic group in all three hypothermic groups (P<0.05 vs. 37°C). Coronary flow during reperfusion was higher in all three groups of hypothermic hearts and was slightly, but not significantly, higher after 45 min of reflow at 27°C than 20°C or 10°C. The results of this study demonstrate that myocardial preservation is optimal when hearts are cooled to 27°C during the ischemic period. Further cooling of the heart to 20°C or 10°C, while resulting in less accumulation of carbon dioxide in the myocardium, results in no additional protection of ventricular function. These data suggest that in the clinical setting, profound cooling of hearts during 'ischemic arrest' may offer no more myocardial protection than does moderate hypothermia.