Basal metabolic energy requirements of polarized and depolarized arrest in rat heart
Sternbergh, W.C.; Brunsting, L.A.; Abd-Elfattah, A.S.; Wechsler, A.S.
American Journal of Physiology 256(3 Pt 2): H846-H851
1989
ISSN/ISBN: 0002-9513 PMID: 2923243 Document Number: 344181
Basal energy requirements of polarized [tetrodotoxin (TTX), 25 .mu.m] and depolarized [potassium (K), 20 mM] arrested hearts were studied by continuously measuring myocardial oxygen consumption (M.ovrhdot.VO2) 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. (M.ovrhdot.V)2 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.cntdot.min-1.cntdot.g dry wt-1, P < 0.001). Coronary flow was lower in the polarized group (14.3 .+-. 1.4 vs. 28.4 .+-. 2.2 ml.cntdot.min-1.cntdot.g dry wt-1, P < 0.001, data at 30 min of arrest), but flow-restricted studies showed basal M.ovrhdot.VO2 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 < 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.