| Nitric oxide and liver microcirculation during autoregulation and haemorrhagic shock in rabbit model. | |
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MedLine Citation:
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PMID: 16613926 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Direct evidence of nitric oxide (NO) involvement in the regulation of hepatic microcirculation is not yet available under physiological conditions nor in haemorrhagic shock. METHODS: A laser Doppler flowmetry was used to measure liver perfusion index and a specific NO-sensitive electrode was inserted into liver parenchyma of anaesthetized rabbits. Hepatic autoregulation during moderate hypovolaemia {mean arterial pressure at 50 mm Hg without liver perfusion alteration; blood withdrawal 17.7 (4.2) ml [mean (SD)]} or haemorrhagic shock [mean arterial pressure at 20 mm Hg associated with liver perfusion impairment and lactic acidosis; blood withdrawal 56.0 (6.8) ml] were investigated over 60 min and were followed by a rapid infusion of the shed blood. Involvement of NO synthases was evaluated using a non-specific inhibitor, NAPNA (Nomega-nitro-L-arginine P-nitro-anilide). RESULTS: In the autoregulation group, a decrease [30.0 (4.0) mm Hg] of mean arterial pressure did not alter liver perfusion index, whereas the liver NO concentration increased and reached a plateau [125 (10)%; compared with baseline; P<0.05]. This NO concentration was reduced to zero by the administration of NO synthase inhibitor. Haemorrhagic shock led to a rapid decrease in liver perfusion index [60 (7)%; compared with baseline; P<0.05] before an immediate and continuous increase in NO concentration [250 (50)%; compared with baseline; P<0.05]. Infusion of NO inhibitor before haemorrhagic shock reduced the NO concentration to zero and hepatic perfusion by 60 (8)% (P<0.05) of the baseline. Mean arterial pressure increased simultaneously. In these animals, during haemorrhage, a continuous increase in NO concentration still occurred and liver perfusion slightly increased. In all groups but NAPNA+haemorrhagic shock, blood replacement induced recovery of baseline values. CONCLUSIONS: NO plays a physiological role in the liver microcirculation during autoregulation. Its production is enzyme-dependent. Conversely, haemorrhagic shock induces a rapid increase in hepatic NO that is at least partially enzyme-independent. |
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Authors:
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F Lhuillier; M-O Robert; P Crova; J Goudable; F Arnal; R Cespuglio; G Annat; J-P Viale |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-04-13 |
Journal Detail:
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Title: British journal of anaesthesia Volume: 97 ISSN: 0007-0912 ISO Abbreviation: Br J Anaesth Publication Date: 2006 Aug |
Date Detail:
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Created Date: 2006-07-11 Completed Date: 2006-08-21 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0372541 Medline TA: Br J Anaesth Country: England |
Other Details:
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Languages: eng Pagination: 137-46 Citation Subset: IM |
Affiliation:
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Département d'Anesthésie-Réanimation, Hôpital de la Croix Rousse, 103 Grande Rue de la Croix-Rousse, 69317 Lyon Cedex 04, France. franck.lhuillier@chu-lyon.fr |
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| MeSH Terms | |
Descriptor/Qualifier:
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Anilides
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administration & dosage Animals Arginine / administration & dosage, analogs & derivatives Blood Pressure / physiology Carbon Dioxide / physiology Disease Models, Animal Hepatic Artery / physiology Homeostasis / physiology* Infusions, Intravenous Liver / blood supply*, physiology Microcirculation Models, Animal Nitric Oxide / analysis, biosynthesis* Nitric Oxide Synthase / antagonists & inhibitors Oxygen / physiology Rabbits Shock, Hemorrhagic / metabolism, physiopathology* |
| Chemical | |
Reg. No./Substance:
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0/Anilides; 10102-43-9/Nitric Oxide; 124-38-9/Carbon Dioxide; 74-79-3/Arginine; 7782-44-7/Oxygen; 85697-89-8/N(G)-nitroarginine-4-nitroanilide; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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