| Endothelial dysfunction and decreased production of nitric oxide in the intrahepatic microcirculation of cirrhotic rats. | |
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MedLine Citation:
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PMID: 9755227 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Increased intrahepatic resistance in cirrhotic livers is in part caused by increased vascular tone. Several morphological abnormalities have been described in the sinusoidal endothelial cells of cirrhotic livers, but the functional impact of these abnormalities on the intrahepatic vascular tone has not been studied. The aim of this study was to investigate the intrahepatic endothelial function and the role of nitric oxide (NO) with regard to vascular tone in cirrhotic livers. Isolated rat liver perfusions were performed in cirrhotic rats (induced by chronic carbon tetrachloride inhalation) and weight-matched normal controls. After preconstricting the intrahepatic microcirculation with methoxamine (10(-4) mol/L), response to cumulative doses of receptor-mediated endothelial agonist, acetylcholine (10(-7) mol/L-10(-5) mol/L), was obtained. In another series, response to the receptor-independent endothelial agonist, calcium ionophore A23187 (10(-7) mol/L and 3 x 10(-7) mol/L), was obtained in the absence and presence of Nomega-nitro-L-arginine (NNA) and indomethacin. In a third series of rats, nitrate and nitrite production was measured in the perfusate of perfused normal and cirrhotic livers. There was significantly less vasorelaxation in cirrhotic livers as compared with normal livers in response to acetylcholine and calcium ionophore A23187 (P < .0001). The impaired vasorelaxation was a result of a decrease in both NO-mediated and non-NO-mediated components of vasorelaxation. Cirrhotic livers from ascitic rats had significantly less vasorelaxation as compared with livers from nonascitic rats (P < .005). There was significantly less production of nitrates and nitrites in cirrhotic livers (P < .05). The liver microcirculation of cirrhotic livers is characterized by endothelial dysfunction that results in impaired release of endothelial relaxing factors including NO. |
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Authors:
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T K Gupta; M Toruner; M K Chung; R J Groszmann |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: Hepatology (Baltimore, Md.) Volume: 28 ISSN: 0270-9139 ISO Abbreviation: Hepatology Publication Date: 1998 Oct |
Date Detail:
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Created Date: 1998-11-05 Completed Date: 1998-11-05 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8302946 Medline TA: Hepatology Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 926-31 Citation Subset: IM |
Affiliation:
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Hepatic Hemodynamic Laboratory, VA Medical Center, West Haven, CT 06516, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Animals Calcimycin / pharmacology Carbon Tetrachloride Poisoning / complications Endothelium, Vascular / physiology, physiopathology* Indomethacin / pharmacology Liver Circulation / physiology* Liver Cirrhosis, Experimental / blood, chemically induced, physiopathology* Male Methoxamine / pharmacology Microcirculation / drug effects, physiology, physiopathology* Muscle, Smooth, Vascular / drug effects, physiology, physiopathology Nitrates / blood Nitric Oxide / biosynthesis* Nitrites / blood Nitroarginine / pharmacology Perfusion Rats Rats, Sprague-Dawley Reference Values Vasodilation / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Nitrates; 0/Nitrites; 10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine; 390-28-3/Methoxamine; 51-84-3/Acetylcholine; 52665-69-7/Calcimycin; 53-86-1/Indomethacin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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