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AJP - Heart and Circulatory Physiology, Vol 256, Issue 3 846-H851, Copyright © 1989 by American Physiological Society
ARTICLES |
W. C. Sternbergh, L. A. Brunsting, A. S. Abd-Elfattah and A. S. Wechsler
Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710.
Basal energy requirements of polarized [tetrodotoxin (TTX), 25 microns] and depolarized [potassium (K), 20 mM] arrested hearts were studied by continuously measuring myocardial oxygen consumption (MVO2) during 60 min of normothermic arrest in isolated Langendorff-perfused rat hearts. TTX, a fast sodium channel blocker, was used to produce polarized arrest because of its specificity and reversibility. MVO2 was significantly lower in the polarized (TTX) group at all time points, a typical difference occurring 30 min after arrest (0.070 +/- 0.005 vs. 0.109 +/- 0.006 ml O2.min-1.g dry wt-1, P less than 0.001). Coronary flow was lower in the polarized group (14.3 +/- 1.4 vs. 28.4 +/- 2.2 ml.min-1.g dry wt-1, P less than 0.001, data at 30 min of arrest), but flow-restricted studies showed basal MVO2 to be independent of variation in coronary flow within this range. Recovery of function was similar in both groups. Ventricular pressure during cardiac arrest was lower in the polarized group (5.5 +/- 1.2 vs. 10.3 +/- 1.3 mmHg, P less than 0.01, data at 30 min of arrest), implying reduced myocardial wall tension and a lower intracellular calcium concentration. These results suggest that polarized arrest can decrease myocardial metabolic demands below that of depolarized arrest. A plausible mechanism is a reduction in myocardial wall tension caused by decreased calcium influx mediated by the Na-Ca exchanger.
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