SUMMARYWe assessed the effects of ethanol and autonomic blockade on left ventricular function in nine normal subjects, age 20-35 years, using M-mode echocardiography and systolic time intervals. On day 1, measurements were made of heart rate, mean velocity of circumferential fiber shortening, and left ventricular preejection period and left ventricular ejection time ratio (PEP/LVET), during a control period and after autonomic blockade. Autonomic blockade was produced with intravenous propranolol (0.2 mg/kg body weight) and atropine (0.04 mg/kg body weight). On day two, measurements were again made during a control period, then with ethanol alone, followed by addition of autonomic blockade to ethanol. One hundred eighty milliliters of ethanol were ingested over 60 minutes, resulting in a mean blood ethanol level of 110 mg/dl (range 77-135 mg/dl) at 60 minutes post-ingestion.There were no significant differences between the control data on days 1 and 2. Blood pressure was unchanged throughout the study. On day 1, autonomic blockade alone resulted in the expected increase in heart rate (p < 0.001), with a proportional increase in mean velocity of circumferential fibr shortening (p < 0.01), and an increase in PEP/LVET (p < 0.01). On day 2, ethanol alone resulted in no significant changes except for a slight increase in PEP/LVET (p < 0.02). Ethanol plus autonomic blockade, (day 2), compared with autonomic blockade alone (day 1), revealed a decrease in mean velocity of circumferential fiber shortening (p < 0.05), and an increase in PEP/LVET (p < 0.01), with a decrease in intrinsic heart rate (p < 0.001).We conclude that in normal subjects: 1) autonomic blockade does not directly affect contractility; 2) acute ethanol ingestion alone does not produce important changes in cardiac function; and, 3) ethanol in the autonomic blockaded heart causes a significant decrease in contractility. Thus, we infer that ethanol has a negative inotropic effect which is masked by catecholamines and/or autonomic nervous system discharge.CHRONIC INGESTION OF ETHANOL is known to cause cardiac dysfunction, most notably as congestive cardiomyopathy.'-5 Cardiac function, as measured by systolic time intervals, may be depressed even in the clinically "normal" alcoholic.6 In addition, patients with coronary heart disease have shown depressed hemodynamics,78 as well as decreased exercise tolerance with increased ischemic ST-segment abnormalities and angina,9 after acute oral ingestion of moderate amounts of ethanol. Intravenous administration of ethanol to dogs caused decreased coronary flow and increased coronary resistance at all dosage levels.10 However, the acute administration of ethanol to dogs and to normal humans has resulted in conflicting reports of the effects on left ventricular (LV) function. Autonomic blockade may therefore unmask myocardial dysfunction during ethanol ingestion. We therefore extended the study of the effects of acute ethanol ingestion on LV function in normal subjects to include autonomic blockade.28' 29 Because of...
