Circulating levels of neuropeptides (cgrp, vip, npy) in patients with fulminant hepatic failure

doi:10.1054/npep.2001.0861

Neuropeptides

Volume 35, Issues 3–4, June 2001, Pages 174-180

https://doi.org/10.1054/npep.2001.0861 Get rights and content

Abstract

The present study investigated the circulating levels and cerebral fluxes of calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), and neuropeptide Y (NPY) and their relation to cerebral blood flow (CBF) during normoventilation and hyperventilation in patients with fulminant hepatic failure (FHF). Sixteen patients with FHF were studied and compared to six patients with cirrhosis of the liver. CBF was measured by the ¹³³Xe wash-out technique. Blood samples were obtained simultaneously from the artery and internal jugular bulb. Concentrations of CGRP and VIP were higher in FHF than in cirrhosis, 87 (55–218) vs 29 (21–42) pmol/L, and 11 (6–29) vs 5 (3–9) pmol/L, respectively. NPY was normal, none of the measures were related to CBF, and there was no detectable net brain fluxes. Hyperventilation did not alter any of the measures. CGRP and VIP in FHF seem to reflect hemodynamic changes in the systemic rather than in the cerebral circulation.

References (36)

JM Allen et al.
Presence of neuropeptide Y in human circle of Willis and its possible role in cerebral vasospasm
Lancet
(1984)
DT Beattie et al.
The influence of neurokinins and calcitonin gene-related peptide on cerebral blood flow in anaesthetized guinea-pigs
Neuropeptides
(1993)
F Bendtsen et al.
Increased circulating calcitonin gene-related peptide (CGRP) in cirrhosis
J Hepatol
(1991)
AT Blei et al.
Pathophysiology of cerebral edema in fulminant hepatic failure
J Hepatol
(1999)
PJ Goadsby et al.
Examination of the involvement of neuropeptide Y (NPY) in cerebral autoregulation using the novel NPY antagonist PP56
Neuropeptides
(1993)
CS Humphrey et al.
Hepatic and pulmonary clearance of exogenous vasoactive intestinal peptide in the rat
Gastroenterology
(1979)
D Hvidsten et al.
Clearance of vasoactive intestinal polypeptide (VIP) in the porcine pulmonary circulation
Regul Pept
(1989)
GM Knudsen et al.
Blood-brain barrier permeability in galactosamine-induced hepatic encephalopathy. No evidence for increased GABA-transport
J Hepatol
(1988)
FS Larsen et al.
Functional loss of cerebral blood flow autoregulation in patients with fulminant hepatic failure
J Hepatol
(1995)
G Strauss et al.
Hyperventilation restores cerebral blood flow autoregulation in patients with acute liver failure
J Hepatol
(1998)

R Uddman et al.

Calcitonin gene-related peptide (CGRP): perivascular distribution and vasodilatory effects

Regul Pept

(1986)

S Aggarwal et al.

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: a retrospective study

Hepatology

(1994)

T Almdal et al.

Cerebral blood flow and liver function in patients with encephalopathy due to acute and chronic liver diseases

Scand J Gastroenterol

(1989)

W Bernhard et al.

Degradation of vasoactive intestinal peptide by isolated, ventilated, and perfused rat lungs

Eur J Clin Invest

(1989)

KG Braslis et al.

Pharmacokinetics and organ-specific metabolism of calcitonin gene-related peptide in sheep

J Endocrinol

(1988)

AM Ebeid et al.

Hepatic inactivation of vasoactive intestinal peptide in man and dog

Ann Surg

(1978)

DF Gardner et al.

Preferential binding of vasoactive intestinal peptide to hepatic nonparenchymal cells

Am J Physiol

(1985)

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REGULAR ARTICLECirculating levels of neuropeptides (cgrp, vip, npy) in patients with fulminant hepatic failure

Abstract

Lancet

Neuropeptides

J Hepatol

J Hepatol

Neuropeptides

Gastroenterology

Regul Pept

J Hepatol

J Hepatol

J Hepatol

Regul Pept

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: a retrospective study

Hepatology

Cerebral blood flow and liver function in patients with encephalopathy due to acute and chronic liver diseases

Scand J Gastroenterol

Degradation of vasoactive intestinal peptide by isolated, ventilated, and perfused rat lungs

Eur J Clin Invest

Pharmacokinetics and organ-specific metabolism of calcitonin gene-related peptide in sheep

J Endocrinol

Hepatic inactivation of vasoactive intestinal peptide in man and dog

Ann Surg

Preferential binding of vasoactive intestinal peptide to hepatic nonparenchymal cells

Am J Physiol

REGULAR ARTICLE
Circulating levels of neuropeptides (cgrp, vip, npy) in patients with fulminant hepatic failure