Liver hypermetabolism during alcohol withdrawal in humans. Role of sympathetic overactivity.
Catecholamines, which are elevated during alcohol withdrawal, can alter hepatic blood flow and increase hepatic oxygen consumption. We hypothesized that, in the withdrawal state, hepatic oxygen consumption and delivery could be altered in relation to an increased sympathetic activity. Thirteen chronic alcoholics were studied 34-72 h after withdrawal and 10 days later (control period) using conventional hemodynamic methods. As compared with the control period, splanchnic oxygen uptake was elevated at withdrawal (74.5 +/- 27.1 vs. 59.2 +/- 16.8 ml/min, p less than 0.025) and its variation was correlated with that of plasma epinephrine (r = 0.70, p less than 0.01). The hepatic venous oxygen content was reduced at withdrawal (113 +/- 22 vs. 126 +/- 21 ml/L, p less than 0.025) and correlated inversely with plasma norepinephrine levels (r = 0.56, p less than 0.01). We conclude that, during alcohol withdrawal in humans, hepatic energy expenditure may be elevated in relation to epinephrine secretion and that sympathetic overactivity may hinder the adaptive response in hepatic blood flow. The wide range in sympathetic nervous response to alcohol withdrawal could explain some differences in individual susceptibility to liver damage caused by alcohol.
Hadengue
A
A
Unité de Recherches de Physiopathologie Hépatique (INSERM U 24), Clichy, France.
Moreau
R
R
Lee
S S
SS
Gaudin
C
C
Rueff
B
B
Lebrec
D
D
D004734:Energy Metabolism; D004837:Epinephrine / Q000097:blood; D000431:Ethanol / Q000009:adverse effects*; D006801:Humans; D008099:Liver / Q000378:metabolism*; D008102:Liver Circulation; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption; D013375:Substance Withdrawal Syndrome / Q000378:metabolism* / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D000431:Ethanol; D009638:Norepinephrine; D004837:Epinephrine