| Vascular arginase contributes to arteriolar endothelial dysfunction in a rat model of hemorrhagic shock. | |
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MedLine Citation:
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PMID: 20699748 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Hemorrhagic shock causes hypoperfusion of peripheral tissues and promotes endothelial dysfunction, which may lead to further tissue injury. Trauma increases extrahepatic activity of arginase, an enzyme which competes for l-arginine with nitric oxide synthase, and plays a key role in the development of endothelial dysfunction during aging, hypertension, and diabetes. However, the role of arginase in hemorrhage-induced endothelial dysfunction has not been studied. This study tests the hypothesis that arginase inhibition improves endothelial function after hemorrhage. METHODS: Male Sprague-Dawley rats were implanted with indwelling arterial catheters for blood pressure measurements and blood removal. Awake animals were subjected to a 45% fixed volume controlled hemorrhage and blood pressure was monitored. Unbled rats served as controls. Skeletal muscle arterioles were isolated 24 hours after hemorrhage and cannulated in a pressure myograph system. To study endothelial function, arterioles were exposed to constant midpoint, but altered endpoint pressures, to establish graded levels of luminal flow and internal diameter was measured. RESULTS: Hemorrhage lowered mean arterial pressure that spontaneously recovered to 78% and 88% of baseline in 2 hours and 20 hours, respectively. Vascular arginase II and blood glucose levels were elevated, whereas hemoglobin and insulin levels were decreased 24 hours after blood loss. In posthemorrhage arterioles, flow-induced dilation was abolished. Acute in vitro treatment with an inhibitor of arginase, N-hydroxy-nor-l-arginine, restored flow-induced dilation to unbled control levels. Similarly, the arginase and nitric oxide synthase substrate, l-arginine, but not the inactive isomer, d-arginine, restored flow-induced dilation. CONCLUSIONS: These results indicate that arginase contributes to endothelial dysfunction in resistance vessels after significant hemorrhage. |
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Authors:
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Robert A Johnson; William Durante; Teresa Craig; Kelly J Peyton; John G Myers; Ronald M Stewart; Fruzsina K Johnson |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: The Journal of trauma Volume: 69 ISSN: 1529-8809 ISO Abbreviation: J Trauma Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-11 Completed Date: 2010-09-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0376373 Medline TA: J Trauma Country: United States |
Other Details:
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Languages: eng Pagination: 384-91 Citation Subset: AIM; IM |
Affiliation:
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Division of Trauma and Emergency Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arginase / antagonists & inhibitors, metabolism* Arginine / metabolism Blood Flow Velocity Disease Models, Animal Endothelium, Vascular / enzymology* Enzyme Inhibitors / pharmacology Male Nitric Oxide Synthase / metabolism* Random Allocation Rats Rats, Sprague-Dawley Risk Factors Shock, Hemorrhagic / enzymology* Vascular Resistance / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL74966/HL/NHLBI NIH HHS; R01 HL76187/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase; EC 3.5.3.1/Arginase |
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