ArticleJournal of applied physiology (Bethesda, Md. : 1985)2014
Impact of increased hematocrit on right ventricular afterload in response to chronic hypoxia.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Safety and Efficacy of Therapeutic Erythrocytapheresis Treatment in Chronic Mountain Sickness Patients in Shigatse, Tibet, China.Medical science monitor : international medical journal of experimental and clinical research · 2020Trial
- Slow and fast locomotor muscle adaptations to sustained intermittent hypoxaemia.The journal of physiological sciences : JPS · 2026Article
- Characteristics associated with left ventricular diastolic dysfunction and its prognostic implication in patients with sepsis: a prospective cohort study.Journal of anesthesia · 2026Article
- [U-shaped association between hematocrit and resting pulse oxygen saturation in Tibetan plateau population].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Jagged 2 inhibition attenuates hypoxia-induced mitochondrial damage and pulmonary hypertension through Sirtuin 1 signaling.PloS one · 2024Article
- 3'UTR shortening of HAS2 promotes hyaluronan hyper-synthesis and bioenergetic dysfunction in pulmonary hypertension.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Effects of Red Blood Cell Sickling on Right Ventricular AfterloadExperimental mechanics · 2021Article
- Multiscale structure-function relationships in right ventricular failure due to pressure overload.American journal of physiology. Heart and circulatory physiology · 2018Article
- Impact of chronic hypoxia on proximal pulmonary artery wave propagation and mechanical properties in rats.American journal of physiology. Heart and circulatory physiology · 2018Article
- Estrogen maintains mitochondrial content and function in the right ventricle of rats with pulmonary hypertension.Physiological reports · 2017Article
- Pulmonary vascular collagen content, not cross-linking, contributes to right ventricular pulsatile afterload and overload in early pulmonary hypertension.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Vorticity is a marker of diastolic ventricular interdependency in pulmonary hypertension.Pulmonary circulation · 2016Article
- Increased Red Blood Cell Stiffness Increases Pulmonary Vascular Resistance and Pulmonary Arterial Pressure.Journal of biomechanical engineering · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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, ∼500 μl of blood were extracted and replaced with an equal volume of hydroxyethylstarch to normalize hematocrit and all hemodynamic measurements were repeated. In addition, ∼500 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.
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