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Left ventricular function during alcohol intoxication and autonomic nervous blockade
Authors:H Kelbaek  T Gj?rup  O J Hartling  J Marving  N J Christensen  J Godtfredsen
Affiliation:1. Department of Cardiology, Faculty of Health, Medicine, and Life Sciences, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands;2. Institute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany;3. Montréal Heart Institute, University de Montréal, Montréal, QC, Canada;4. Department of Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, TX, United States;1. GIMSC, Universidad de San Buenaventura, Medellín, Colombia;2. MATBIOM, Universidad de Medellín, Medellín, Colombia;3. Department of Electrical Engineering, Institute of Engineering, Polytechnic of Porto, Porto, Portugal
Abstract:Eight healthy young subjects (6 men, 2 women) entered a controlled investigation of left ventricular (LV) function during alcohol intoxication and autonomic nervous blockade. Radionuclide cardiography was performed at rest and during upright 50% submaximal bicycle exercise. During alcohol intoxication alone (serum ethanol 30 mmol/liter), heart rate at rest increased by 11% (p less than 0.05) and LV ejection fraction (EF) decreased by 6% because of end-systolic dilation. No significant alcohol-induced hemodynamic changes were observed during exercise. Plasma norepinephrine concentration increased by 29% (p less than 0.05), whereas plasma epinephrine concentration did not change. During subsequent autonomic nervous blockade with intravenous metoprolol and atropine infusion, heart rate at rest further increased and systolic blood pressure decreased. These changes were not, however, significantly different from those of a control experiment in which a nonalcoholic isocaloric drink was substituted for alcohol. Plasma norepinephrine levels at rest and during exercise were 25% and 32% higher (both p less than 0.05), respectively, than those during control conditions. Plasma epinephrine concentrations did not change. These findings suggest that alcohol intoxication has a depressant effect on LV function at rest that stimulates autonomic nervous blockade. The increased sympathetic nervous activity during exercise appears to be a toxic rather than a compensatory effect of alcohol.
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