MECHANICAL AND BIOCHEMICAL EFFECTS OF TRANSIENT MYOCARDIAL ISCHEMIA

Global myocardial ischemia was studied in 10 dogs on total cardiopulmonary bypass for periods of 20 min under normothermia and moderate hyperthermia (28°C). Ventricular performance before and after ischemic arrest was assessed by graded distention of an intraventricular balloon and correlated with subcellular function of the sarcoplasmic reticulum and myofibrils. Peak systolic and end-diastolic forces showed no significant differences between prearrest and postarrest values in both groups. Left ventricular pressure work was consistently lower following ischemic arrest under normothermia but the values did not reach statistical significance. No difference in pre- and postarrest values was seen in the hypothermic group. Subcellular function was evaluated by isolating the sarcoplasmic reticulum (SR) and myofibrils from the endocardial and epicardial portions of the free wall of the left ventricle by differential centrifugation. Global myocardial ischemia under normothermic conditions was associated with a significant depression of both SR calcium uptake and myofibrillar ATPase activity from the endocardium. Epicardial myofibrillar ATPase activity was not significantly different in the two groups (normothermic vs hypothermic) and SR calcium uptake was only slightly depressed in the normothermic group. In contrast, both myofibrillar ATPase activity and SR calcium uptake from the endocardium of the hypothermic preparations demonstrated significantly higher activity when compared to the normothermic group. It is concluded that normothermic arrest for 20 min results in a depression of the subcellular functions responsible for the regulation of myocardial contractility and that hypothermic arrest is capable of protecting the endocardial myofibrillar ATPase activity and SR calcium uptake during global ischemia. Therefore myocardial protection afforded by hypothermia seems warrented even for relatively brief periods of clinical ischemic arrest. © 1979.