Prolonged Feeding of Ethanol to the Young Growing Guinea Pig. II. A Model to Study the Effects of Severe Ischemia on Cardiac Protein Synthesis

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Abstract
Although acute perfusion of guinea pig hearts with ethanol does not affect cardiac protein synthesis, the latter is inhibited after prolonged ingestion of ethanol when tested in an in vitro system with the working right ventricle. The added stress of ischemia on such hearts was studied. Hearts were removed from maturing guinea pigs after 13 to 16 wk of ingesting 10% ethanol and were perfused in vitro under conditions of relative ischemia (1/6 of normal coronary flow) with maintenance of right ventricular load and outflow resistance identical to normal pre-ischemic levels. With this degree of ischemia, there was a 4- to 6-fold increase in lactate production, an 80% drop in ATP and a 90% decrease in creatine phosphate after 150 min of the ischemia. Incorporation of both labeled Lys and Phe into cardiac protein was also diminished to 35% of control in the left ventricle and 55% of control in the right. This diminution of protein synthesis was the same in hearts from ethanol-drinking and matched control animals. Thus, prior prolonged ingestion of ethanol did not worsen the inhibition of protein synthesis by O2 deprivation. There were 2 significant differences in hemodynamic response to the ischemia by the right ventricles of hearts from ethanol-drinking guinea pigs compared to their matched controls: a decreased ability of the ventricles to maintain the same peak systolic pressure as the controls during ischemia (4.8 .+-. 0.8 mm Hg compared to 7.5 .+-. 0.06, P < 0.02) and a significant increase in coronary resistance in hearts from ethanol-drinking animals as the ischemic perfusion progressed (coronary pressure 23.6 .+-. 1.3 mm Hg compared to 17.0 .+-. 0.8 in controls, P < 0.001). Although contractility of hearts from ethanol-consuming animals may not show impairment of contraction under normal conditions, the imposition of another stress such as ischemia may expose a contractile deficiency.