Cardiac Effects of Acute Ethanol Ingestion Unmasked by Autonomic Blockade

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Abstract

SUMMARY

We 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 lt; 0.001), with a proportional increase in mean velocity of circumferential fibr shortening (p lt; 0.01), and an increase in PEP/LVET (p lt; 0.01). On day 2, ethanol alone resulted in no significant changes except for a slight increase in PEP/LVET (p lt; 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 lt; 0.05), and an increase in PEP/LVET (p lt; 0.01), with a decrease in intrinsic heart rate (p lt; 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.

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