TY - JOUR
T1 - Left ventricular function during alcohol intoxication and autonomic nervous blockade
AU - Kelbaek, Henning
AU - Gjørup, Thomas
AU - Hartling, Ole J.
AU - Marving, Jens
AU - Christensen, Niels Juel
AU - Godtfredsen, John
PY - 1987/3/1
Y1 - 1987/3/1
N2 - 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 <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 <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 <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 simulates autonomic nervous blockade. The increased sympathetic nervous activity during exercise appears to be a toxic rather than a compensatory effect of alcohol.
AB - 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 <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 <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 <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 simulates autonomic nervous blockade. The increased sympathetic nervous activity during exercise appears to be a toxic rather than a compensatory effect of alcohol.
UR - https://www.scopus.com/pages/publications/0023101463
U2 - 10.1016/0002-9149(87)91193-3
DO - 10.1016/0002-9149(87)91193-3
M3 - Article
C2 - 3825913
AN - SCOPUS:0023101463
SN - 0002-9149
VL - 59
SP - 685
EP - 688
JO - The American Journal of Cardiology
JF - The American Journal of Cardiology
IS - 6
ER -