| Hemodilution does not alter the coronary vasodilating effects of endogenous or exogenous nitric oxide. | |
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MedLine Citation:
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PMID: 18676385 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Introduction: It is well known that hemoglobin is a scavenger of nitric oxide (NO). The present study used a canine model to test the hypothesis that acute normovolemic hemodilution (ANH) affects NO-mediated coronary vasodilation. METHODS: Studies were performed in 18 open-chest, anesthetized dogs. In Series 1, the contribution of endogenous NO to coronary vasodilatation during ANH with 5% dextran-40 (reduction in hematocrit by 50%) was assessed. This was accomplished by comparing myocardial blood flow (MBF; radioactive microspheres) in the left anterior descending (LAD) region, which was treated with the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), to that in the circumflex (control) region. In Series 2, the LAD was perfused via a controlled-pressure extracorporeal system with coronary blood flow (CBF) measured with an ultrasonic, transit-time flow transducer. The dose-dependent increases in CBF caused by acetylcholine (ACh), which releases endogenous NO from the vascular endothelium, and sodium nitroprusside (SNP), which provides exogenous NO, were compared before and during ANH. RESULTS: Acute normovolemic hemodilution caused similar (approximately twofold) increases in MBF (P < 0.01) in the absence and presence of L-NAME, and it did not affect the dose-related increases in CBF caused by ACh and SNP. CONCLUSIONS: Series 1: under baseline conditions, hemoglobin in red blood cells does not limit the coronary vasodilatation resulting from tonic release of NO; NO does not mediate coronary vasodilation during ANH. Series 2: ANH does not influence the coronary vasodilating effects of increased levels of NO, whether due to endogenous release (ACh) or infusion of an NO donor (SNP). |
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Authors:
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George J Crystal; Mohammad El-Orbany; Xiping Zhou; M Ramez Salem; Song-Jung Kim |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Canadian journal of anaesthesia = Journal canadien d'anesthésie Volume: 55 ISSN: 0832-610X ISO Abbreviation: Can J Anaesth Publication Date: 2008 Aug |
Date Detail:
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Created Date: 2008-08-04 Completed Date: 2008-12-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8701709 Medline TA: Can J Anaesth Country: Canada |
Other Details:
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Languages: eng Pagination: 507-14 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, Advocate Illinois Masonic Medical Center, University of Illinois College of Medicine, Chicago, IL 60657 USA. gcrystal@uic.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Adenosine / pharmacology Animals Blood Gas Analysis Blood Pressure / drug effects Coronary Vessels / drug effects*, radionuclide imaging Dogs Enzyme Inhibitors / pharmacology Female Free Radical Scavengers / pharmacology Heart Rate / drug effects Hemodilution / adverse effects*, methods Male Models, Animal NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide* / pharmacology, physiology Nitric Oxide Synthase / antagonists & inhibitors* Nitroprusside / pharmacology Treatment Outcome Vasodilator Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 0/Free Radical Scavengers; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-84-3/Acetylcholine; 58-61-7/Adenosine; 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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