Mechanical and Subcellular Function of Rat Myocardium during Chronic Ethanol Consumption

Abstract

Hemodynamic, mechanical, and subcellular function in a rat model of chronic ethanol consumption (A) and pair-fed control rats (C) were evaluated over a 17-week course. Between 5 and 17 weeks, isovolumetric peak systolic pressure did not change (C = 260 ± 20 mmHg; A = 265 ± 35 mmHg;p > 0.1). At 17 weeks myocardial contractility as evaluated by (dP/dt-max)/32 x LVP began to decline in the A rats (Vmax = 1.46 ± 0.12, r = 0.89; C = 1.560 ± 0.09, r = 0.95) but this is not statistically significant. Neither the velocity of calcium uptake by the isolated sarcoplasmic reticulum (SR) nor the whole heart homogenate (H) was different between C and A rats during the 17-week period and the estimated quantitative content of SR/g Heart did not change (at 17 weeks: mg SR/g Heart = 0.15, C and A). Utilizing Triton X-100 purification of cardiac myofibrils, Mg2+-dependent, Ca2+-stimulated myofribrillar ATPase activity began to decline at 11 weeks (A = 80% of control) and continued to decline at 17 weeks (A = 72% of control). These data suggest that a depression of contractile protein function may be an early alcohol-induced derangement in myocardial contractility that precedes the onset of significant mechanical dysfunction.