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

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Abstract
Previously reported studies demonstrated that the myocardial protection provided by cooling the heart to 27.degree. C during global ischemia can be improved by the additional use of K cardioplegia. The effect of further lowering of the myocardial temperature below 27.degree. C was studied to determine if additional myocardial protection resulted. Feline heart preparations subjected to 60 min of global ischemia and 45 min of normothermic (37.degree. C) reperfusion were divided into 4 groups: 8 maintained at 37, 27, 20 and 10.degree. C. Myocardial CO2 tension, measured by mass spectrometry, during the 60 min ischemic period rose to 342 .+-. 18 mmHg in 37.degree. C hearts, to 231 .+-. 11 mmHg in 27.degree. C hearts, to 105 .+-. 6 mmHg for 20.degree. hearts, and to 56 .+-. 4 mmHg for 10.degree. C hearts. In all 4 groups myocardial O2 tension fell to comparably low levels (< 10 mmHg) during the ischemic period. Myocardial function, as assessed by peak developed ventricular pressure and dP/dtmax [maximum change in pressure with time] was improved compared to the normothermic group in all 3 hypothermic groups (P < 0.05 vs. 37.degree. C). Coronary flow during reperfusion was higher in all 3 groups of hypothermic hearts and was slightly, but not significantly higher after 45 min of reflow at 27.degree. C than 20.degree. C or 10.degree. C. Myocardial preservation apparently is optimal when hearts are cooled to 27.degree. C during the ischemic period. Further cooling of the heart to 20.degree. C or 10.degree. C, while resulting in less accumulation of CO2 in the myocardium, results in no additional protection of ventricular function. In the clinical setting, profound cooling of hearts during ischemic arrest may offer no more myocardial protection than does moderate hypothermia.