| Cardiovascular benefits in moderate increases of blood and plasma viscosity surpass those associated with lowering viscosity: Experimental and clinical evidence. | |
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MedLine Citation:
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PMID: 20203362 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Decreasing blood viscosity has been proposed since the advent of hemodilution as a means for increasing perfusion in many pathological conditions, and increased plasma viscosity is associated with the presence of pathological conditions. However, experimental studies show that microvascular functions as represented by functional capillary density in conditions of significantly decreased viscosity is impaired, a problem corrected by increasing plasma and blood viscosity. Blood viscosity, primarily dependent on hematocrit (Hct) is a determinant of peripheral vascular resistance, and therefore blood pressure. In the healthy population Hct presents a variability, which is not reflected by the variability of blood pressure. This is due to a regulatory process at the level of the endothelium, whereby the increase of Hct (and therefore blood viscosity) leads to increased shear stress and the production of the vasodilator nitric oxide (NO), a finding supported by experimental studies showing that the acute increase of Hct lowers blood pressure. Studies that in the healthy population show that blood pressure and Hct have a weak positive correlation. However, when the effect of blood viscosity is factored out, blood pressure and Hct are negatively and significantly correlated, indicating that as blood viscosity increases, the circulation dilates. Conversely, lower Hct and blood viscosity conditions lead to a constricted circulation, associated with a condition of decreased NO bioavailability, and therefore a pro-inflammatory condition. |
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Authors:
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B Y Salazar V?zquez; J Martini; A Ch?vez Negrete; A G Tsai; S Forconi; P Cabrales; P C Johnson; M Intaglietta |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Clinical hemorheology and microcirculation Volume: 44 ISSN: 1875-8622 ISO Abbreviation: Clin. Hemorheol. Microcirc. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-03-05 Completed Date: 2010-06-18 Revised Date: 2010-06-24 |
Medline Journal Info:
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Nlm Unique ID: 9709206 Medline TA: Clin Hemorheol Microcirc Country: Netherlands |
Other Details:
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Languages: eng Pagination: 75-85 Citation Subset: IM |
Affiliation:
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Faculty of Medicine, Universidad Ju?rez del Estado de Durango, Victoria de Durango, DGO, Mexico. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Blood Viscosity
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drug effects,
physiology* Cardiovascular Physiological Phenomena Hematocrit Hemodilution / methods* Humans Hypertension / blood Microcirculation / physiology* Nitric Oxide / blood, metabolism Vascular Resistance / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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P01HL071064-05/HL/NHLBI NIH HHS; R01-HL62318/HL/NHLBI NIH HHS; R01-HL62354/HL/NHLBI NIH HHS; R34-HL64395/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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