polycythemia/hypoxia

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Sequence analysis of the 3' hypoxia-responsive element of the human erythropoietin gene in patients with erythrocytosis.

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Erythrocytosis arises from a variety of pathogenic mechanisms. We sequenced a 256-bp region 3' to the erythropoietin (Epo) gene which included a 24- to 50-bp minimal hypoxia-responsive element spanning HIF-1- and HNF-4-binding sites in 12 patients with erythrocytosis and 4 normal subjects. Four

Consequences of moderate hypoxia on red cell glycolytic metabolism in polycythemia rubra vera.

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Red blood cell metabolism was studied in male patients with polycythemia rubra vera (Vaquez disease) and compared to a reference sample of 74 healthy adults. A total of seventeen enzyme activities and seventeen metabolite concentrations were determined. In addition to the modifications of the

Pulmonary vascular adaptations to augmented polycythemia during chronic hypoxia.

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We previously found that augmentation of polycythemia by exogenous human recombinant erythropoietin (EPO) failed to worsen the severity of hypoxic pulmonary hypertension in rats. We asked whether this unexpected finding was related to reductions in cardiac output, left ventricular end-diastolic

Phlebotomy with iron therapy to correct the microcytic polycythemia of chronic hypoxia.

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Patients with chronic hypoxia develop a physiologically appropriate "secondary" polycythemia that improves oxygen carrying capacity. Supplemental iron is often required to maintain this. In severe cases when hematocrit levels approach 70%, iron is withheld in order to avoid dangerously high

Perinatal hypoxia increases susceptibility to high-altitude polycythemia and attendant pulmonary vascular dysfunction.

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Perinatal exposures exert a profound influence on physiological function, including developmental processes vital for efficient pulmonary gas transfer throughout the lifespan. We extend the concept of developmental programming to chronic mountain sickness (CMS), a debilitating syndrome marked by

Association between serum concentrations of hypoxia inducible factor responsive proteins and excessive erythrocytosis in high altitude Peru.

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Painschab, Matthew S., Gary E. Malpartida, Victor G. Davila-Roman, Robert H. Gilman, Todd M. Kolb, Fabiola Leon-Velarde, J. Jaime Miranda, and William Checkley. Association between serum concentrations of hypoxia inducible factor responsive proteins and excessive erythrocytosis in high altitude

A rat model of high altitude polycythemia rapidly established by hypobaric hypoxia exposure.

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OBJECTIVE To investigate the effects of simple hypobaric hypoxia on parameters of hematology and blood rheology in order to establish a rat model of simulated high altitude polycythemia (HAPC) for the study of pathophysiologic mechanisms and medical prevention and treatment of

Does Renal Tubular Injury-Induced Local Tissue Hypoxia Involve Post-Transplantation Erythrocytosis?

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BACKGROUND The pathogenesis of post-transplantation erythrocytosis (PTE) is not well understood and appears to be multifactorial. Our hypothesis in this study was that several factors, including toxicity of calcineurin inhibitor, immunologic factors, and chronic allograft nephropathy, can trigger

[Effect of polycythemia on hypoxia induced pulmonary hypertension and pulmonary vascular remodeling in rats].

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OBJECTIVE To investigate the effect of polycythemia on hypoxia induced pulmonary hypertension and pulmonary vascular remodeling in rats. METHODS The healthy female Sprague-Dawley rats were randomly divided into 3 groups: normoxia control group (C group), hypoxia group (H group), hypoxia + different

Pulmonary artery pressure and iron deficiency in patients with upregulation of hypoxia sensing due to homozygous VHL(R200W) mutation (Chuvash polycythemia).

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BACKGROUND Patients with Chuvash polycythemia, (homozygosity for the R200W mutation in the von Hippel Lindau gene (VHL)), have elevated levels of hypoxia inducible factors HIF-1 and HIF-2, often become iron-deficient secondary to phlebotomy, and have elevated estimated pulmonary artery pressure by

Notch Downregulation and Extramedullary Erythrocytosis in Hypoxia-Inducible Factor Prolyl 4-Hydroxylase 2-Deficient Mice.

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Erythrocytosis is driven mainly by erythropoietin, which is regulated by hypoxia-inducible factor (HIF). Mutations in HIF prolyl 4-hydroxylase 2 (HIF-P4H-2) (PHD2/EGLN1), the major downregulator of HIFα subunits, are found in familiar erythrocytosis, and large-spectrum conditional inactivation of

Decreased "ineffective erythropoiesis" preserves polycythemia in mice under long-term hypoxia.

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Hypoxia induces innumerable changes in humans and other animals, including an increase in peripheral red blood cells (polycythemia) caused by the activation of erythropoiesis mediated by increased erythropoietin (EPO) production. However, the elevation of EPO is limited and levels return to normal

Effect of induced erythrocythemia on hypoxia tolerance during physical exercise.

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The effect of induced erythrocythemia on hypoxia tolerance during physical exercise was determined for five male mountain climbers. Treadmill testing was performed under four conditions: 1) prereinfusion, normoxia (Pre-N); 2) prereinfusion, hypoxia (Pre-H); 3) postreinfusion, normoxia (Post-N); and

von Hippel-Lindau mutation in mice recapitulates Chuvash polycythemia via hypoxia-inducible factor-2alpha signaling and splenic erythropoiesis.

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The R200W mutation in the von Hippel-Lindau (VHL) tumor suppressor protein (pVHL) is unique in that it is not associated with tumor development, but rather with Chuvash polycythemia, a heritable disease characterized by elevated hematocrit and increased serum levels of erythropoietin and VEGF.

Therapeutic Efficacy of Methazolamide Against Intermittent Hypoxia-Induced Excessive Erythrocytosis in Rats.

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Zhang, Zhiqing, Zhonghai Xiao, Bingnan Deng, Xiaohua Liu, Wei Liu, Hongjing Nie, Xi Li, Zhaoli Chen, Danfeng Yang, and Ruifeng Duan. Therapeutic efficacy of methazolamide against intermittent hypoxia-induced excessive erythrocytosis in rats. High Alt Med Biol 19:69-80, 2018.-This study aimed to

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