NDLI: Impact of increased hematocrit on right ventricular afterload in response to chronic hypoxia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Schreier, David A. Hacker, Timothy A. Hunter, Kendall Eickoff, Jens Liu, Aiping Song, Gouqing Chesler, Naomi
Description	Author Affiliation: Schreier DA ( Department of Biomedical Engineering University of Wisconsin, Madison, Wisconson); Hacker TA ( Department of Medicine Medical Science Center, Madison, Wisconsin); Hunter K ( Department of Bioengineering University of Colorado, Aurora, Colorado.); Eickoff J ( Department of Medicine Medical Science Center, Madison, Wisconsin); Liu A ( Department of Biomedical Engineering University of Wisconsin, Madison, Wisconson); Song G ( Department of Medicine Medical Science Center, Madison, Wisconsin); Chesler N ( Department of Biomedical Engineering University of Wisconsin, Madison, Wisconson)
Abstract	Chronic hypoxia causes chronic mountain sickness through hypoxia-induced pulmonary hypertension (HPH) and increased hematocrit. Here, we investigated the impact of increased hematocrit and HPH on right ventricular (RV) afterload via pulmonary vascular impedance. Mice were exposed to chronic normobaric hypoxia (10% oxygen) for 10 (10H) or 21 days (21H). After baseline hemodynamic measurements, â¼500 µl of blood were extracted and replaced with an equal volume of hydroxyethylstarch to normalize hematocrit and all hemodynamic measurements were repeated. In addition, â¼500 µl of blood were extracted and replaced in control mice with an equal volume of 90% hematocrit blood. Chronic hypoxia increased input resistance (Z0 increased 82% in 10H and 138% in 21H vs. CTL; P < 0.05) and characteristic impedance (ZC increased 76% in 10H and 109% in 21H vs. CTL; P < 0.05). Hematocrit normalization did not decrease mean pulmonary artery pressure but did increase cardiac output such that both Z0 and ZC decreased toward control levels. Increased hematocrit in control mice did not increase pressure but did decrease cardiac output such that Z0 increased. The paradoxical decrease in ZC with an acute drop in hematocrit and no change in pressure are likely due to inertial effects secondary to the increase in cardiac output. A novel finding of this study is that an increase in hematocrit affects the pulsatile RV afterload in addition to the steady RV afterload (Z0). Furthermore, our results highlight that the conventional interpretation of ZC as a measure of proximal artery stiffness is not valid in all physiological and pathological states.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
DOI	10.1152/japplphysiol.00059.2014
Journal	Journal of Applied Physiology
Issue Number	8
Volume Number	117
Language	English
Publisher	American Physiological Society
Publisher Date	2014-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Heart Ventricles Physiopathology Anoxia Ventricular Function, Right Physiology Altitude Sickness Animals Blood Pressure Cardiac Output Hematocrit Hypertension, Pulmonary Lung Mice Mice, Inbred C57bl Pulmonary Artery Pulmonary Circulation Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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