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Increased Sympathetic Nervous Activity and the Effects of Its Inhibition with Clonidine in Alcoholic Cirrhosis

Murray Esler, MB, BS, PhD; Frank Dudley, MD; Garry Jennings, MD; Henry Debinski, MB, BS; Gavin Lambert, BSc; Penelope Jones, RN; Brendan Crotty, MB, BS; John Colman, MB, BS; and Ian Willett, MB, BS
[+] Article and Author Information

Grant Support: In part by a National Health and Medical Research Council of Australia Program grant to Drs. Dudley and Willett and by an NHMRC Institute grant to the Baker Medical Research Institute.

Requests for Reprints: Murray Esler, MBBS, PhD: Baker Medical Research Institute, Commercial Road, Prahran 3181, Melbourne, Australia.

Current Author Addresses: Dr. Esler and Mr. Lambert: Baker Medical Research Institute, Commercial Road, Prahran 3181, Melbourne, Australia.

Drs. Dudley, Debinski, Colman, and Ms. Jones: Gastroenterology Service, The Alfred Hospital Commercial Road, Prahran 3181, Australia. Dr. Jennings: Alfred and Baker Medical Unit, Commercial Road, Prahran 3181, Australia.

Dr. Crotty: Gastroenterology Unit, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, United Kingdom.

Dr. Willett: Gastroenterology Service, Dandenong and Distric Hospital, David Street, Dandenong 3175, Australia.


© 1992 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1992;116(6):446-456. doi:10.7326/0003-4819-116-6-446
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Objective: To study disturbances in sympathetic nervous system function in patients with alcoholic cirrhosis and the effect of Clonidine on such disturbances.

Design: Cross-sectional physiologic and neurochemical evaluation of patients with cirrhosis and of healthy controls; an uncontrolled trial of intravenous Clonidine in the cirrhotic patients.

Patients: Forty-four hospitalized patients with biopsy-proven alcoholic cirrhosis and 31 healthy controls.

Interventions: Intravenous clonidine.

Main Outcome Measures: Radiotracer-derived measures of norepinephrine release to plasma, central hemodynamics, wedge hepatic vein pressure, and measures of renal function.

Main Results: In patients with cirrhosis, clonidine reduced previously elevated norepinephrine overflow rates for the whole body, kidneys, and hepatomesenteric circulation. This sympathetic inhibition was accompanied by the following potentially clinically beneficial effects: the lowering of renal vascular resistance (median reduction, 24%; 95% Cl, 14% to 31%), the elevation of glomerular filtration rate (median increase, 27%; Cl, 14% to 39%), and the reduction of portal venous pressure (median reduction, 25%; Cl, 18% to 32%). The norepinephrine and hemodynamic responses to graded clonidine dosing (1, 2, and 3 µg/kg body weight intravenously) indicated that the sympathetic outflow to the hepatomesenteric circulation was more sensitive to pharmacologic suppression with clonidine than was the sympathetic outflow to the systemic circulation.

Conclusions: The sympathetic nerves to the kidneys, heart, and hepatomesenteric circulation are stimulated in patients with cirrhosis. Clonidine inhibits these activated sympathetic outflows differentially, which could possibly provide a basis for the selective pharmacologic treatment of portal hypertension in patients with cirrhosis.

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