Document Detail


Vascular arginase contributes to arteriolar endothelial dysfunction in a rat model of hemorrhagic shock.
MedLine Citation:
PMID:  20699748     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of trauma     Volume:  69     ISSN:  1529-8809     ISO Abbreviation:  J Trauma     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-11     Completed Date:  2010-09-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376373     Medline TA:  J Trauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  384-91     Citation Subset:  AIM; IM    
Affiliation:
Division of Trauma and Emergency Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
R01 HL74966/HL/NHLBI NIH HHS; R01 HL76187/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 74-79-3/Arginine; EC 1.14.13.39/Nitric Oxide Synthase; EC 3.5.3.1/Arginase

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


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