Intravenous ethanol acutely depresses myocardial performance in conscious dogs, independent of autonomic innervation.
Ethanol may depress myocardial performance in dogs; leaves open human translation and clinical relevance.
The cardiac effects of ethanol were studied in six conscious dogs chronically instrumented for measurement of left ventricular pressure, internal transverse diameter, and outflow. Successive intravenous infusions of ethanol produced blood levels of 120 ± 16 ( sem ) mg% (infusion #1) and 311 ± 19 mg% (infusion #2). Stroke volume decreased from 20.1 ± 1.6 ml preinfusion to 17.2 ± 1.9 ml after infusion #1 ( P < 0.01) and 13.6 ± 1.9 ml after infusion #2 ( P < 0.01). Left ventricular end diastolic pressure increased 2.5 mm Hg with infusion #1 ( P < 0.05) and 6.0 mm Hg with infusion #2 ( P < 0.05). Left ventricular dp/dt max fell 17% with infusion #1 ( P < 0.001) and 30% with infusion #2 ( P < 0.01). Left ventricular diameter increased at end diastole and end systole with ethanol. Heart rate was unchanged with infusion #1 and increased with infusion #2; left ventricular systolic pressure was unaltered. Studies after pharmacological autonomic denervation with propranolol and atropine demonstrated changes in left ventricular dp/dt max, left ventricular end diastolic pressure, and stroke volume similar to unblocked results. Thus ethanol at blood levels commonly encountered in social usage is a potent myocardial depressant.
No takes yet. Share an insight, caveat, or question.
Horwitz et al. (1974) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: