Document Detail

Portal vascular responsiveness to sympathetic stimulation and nitric oxide in cirrhotic rats.
MedLine Citation:
PMID:  8836907     Owner:  NLM     Status:  MEDLINE    
AIMS/METHODS: The modulatory role of nitric oxide in portal vasoconstrictor responses was investigated in the isolated perfused liver of cirrhotic rats (induced by carbon tetrachloride/phenobarbitone; n = 6). Age-matched (n = 5) and phenobarbitone-treated rats (n = 5) served as controls. RESULTS: At a constant flow rate of 5 ml/min there was no difference in basal perfusion pressure between the groups. Responses to electrical field stimulation of perivascular nerves caused frequency-dependent increases in perfusion pressure that were not significantly different between the groups. In contrast, dose-dependent vasoconstrictor responses to bolus injections of noradrenaline were up to two-fold greater than those observed in controls (p < 0.05). Vasoconstrictor responses to bolus injections of methoxamine (a selective alpha 1-adrenoceptor agonist) or adenosine 5'-triphosphate (ATP, a cotransmitter with noradrenaline in sympathetic nerves) were dose-dependent and similar between the groups. Infusion of the nitric oxide synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 30 microM) had no effect on basal tone or on responses to electrical field stimulation or injected agents. A step-wise increase in flow to 10, 15 and 20 ml/min produced a similar increase in perfusion pressure within each group. At increased flow, there was a decrease in responsiveness to noradrenaline (5 nmol) in preparations from all groups. In the presence of the K+ channel inhibitor glibenclamide (5 microM), the effect of noradrenaline in the cirrhotic group at flow rates of 5, 10 and 15 ml/min was maintained to a significantly greater extent than in either control group, suggesting that ATP-sensitive K+ channels in the portal venous bed may be activated in cirrhosis. CONCLUSIONS: We conclude that portal vasoconstriction associated with noradrenaline, but not with sympathetic nerve stimulation, methoxamine or ATP, is enhanced in cirrhosis. Nitric oxide does not appear to play a modulatory role in these responses.
R T Mathie; V Ralevic; G Burnstock
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hepatology     Volume:  25     ISSN:  0168-8278     ISO Abbreviation:  J. Hepatol.     Publication Date:  1996 Jul 
Date Detail:
Created Date:  1996-12-12     Completed Date:  1996-12-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8503886     Medline TA:  J Hepatol     Country:  DENMARK    
Other Details:
Languages:  eng     Pagination:  90-7     Citation Subset:  IM    
Department of Surgery, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
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MeSH Terms
Adenosine Triphosphate / pharmacology
Electric Stimulation
Liver Cirrhosis, Experimental / physiopathology*
Methoxamine / pharmacology
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide / physiology*
Norepinephrine / pharmacology
Portal Pressure / drug effects
Portal System / physiopathology*
Rats, Wistar
Sympathetic Nervous System / physiology*
Vasoconstriction / drug effects
Reg. No./Substance:
10102-43-9/Nitric Oxide; 390-28-3/Methoxamine; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-41-2/Norepinephrine; 56-65-5/Adenosine Triphosphate
Erratum In:
J Hepatol 1997 May;26(5):1160-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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