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  • Leiter, J. C.  (5)
  • Ou, L. C.  (5)
  • 1
    Online Resource
    Online Resource
    Pathophysiological effects of hemodilution in chronic mountain sickness in rats
    American Physiological Society ; 1996
    In:  Journal of Applied Physiology Vol. 80, No. 2 ( 1996-02-01), p. 574-582
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 80, No. 2 ( 1996-02-01), p. 574-582
    Abstract: We examined the effect of isovolemic hemodilution in a rat model of chronic mountain sickness (CMS). After 30 days at simulated high altitude (5,500 m), Hilltop rats had developed evidence of CMS: severe hypoxemia, polycythemia, and pulmonary arterial hypertension. Isovolemic hemodilution to a mean hematocrit of 46 +/- 5% was well tolerated by both the hypoxia-sensitive Hilltop rats and the companion Madison rat strain that does not develop CMS. After hemodilution, we found no evidence of sustained improvements in ventilation or gas exchange in either strain. Despite the fall in blood viscosity, cardiac output increased only marginally, and pulmonary arterial hypertension persisted in the Hilltop rats. Vascular hindrance increased after hemodilution, preventing a significant decline in pulmonary and systemic vascular resistances in the Hilltop rats. Blood O2 content and the coefficient of O2 delivery fell after hemodilution, but O2 consumption was sustained at a normal level after hemodilution by increasing the extraction fraction in the Hilltop strain. There was systemic hypotension through the first day of hemodilution, but this was the only apparent adverse effect of hemodilution. We conclude that isovolemic hemodilution was well tolerated despite the reduction in tissue O2 delivery. However, hemodilution failed to improve any of the respiratory and cardiovascular manifestations of CMS in Hilltop rats.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1996.80.2.574
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1996
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 2
    Online Resource
    Online Resource
    Polycythemic responses to hypoxia: molecular and genetic mechanisms of chronic mountain sickness
    American Physiological Society ; 1998
    In:  Journal of Applied Physiology Vol. 84, No. 4 ( 1998-04-01), p. 1242-1251
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 84, No. 4 ( 1998-04-01), p. 1242-1251
    Abstract: We examined erythropoietin (EPO) gene expression and EPO production during hypoxia in two Sprague-Dawley rat strains with divergent polycythemic responses to hypoxia. Hilltop (H) rats develop severe polycythemia, severe hypoxemia, and pulmonary artery hypertension. The H rats often die from a syndrome indistinguishable from chronic mountain sickness (CMS) in humans. Madison (M) rats develop polycythemia and pulmonary artery hypertension that is modest and suffer no excess mortality. We tested the hypothesis that these rat strains have different stimulus-response characteristics governing EPO production. Rats of each strain were exposed to hypoxia (0.5 atm, 73 Torr inspired [Formula: see text]), and renal tissue EPO mRNA and EPO levels, plasma EPO, ventilation, arterial and renal venous blood gases, and indexes of renal function were measured at fixed times during a 30-day hypoxic exposure. During extended hypoxic exposure, H rats had significantly elevated renal EPO mRNA, renal EPO, and plasma EPO levels compared with M rats. Ventilatory responses and indexes of renal function were similar in the strains during the hypoxic exposure. H rats had greater arterial hypoxemia from the onset of hypoxia and more severe renal tissue hypoxemia and greater polycythemia after 14 days of hypoxic exposure. When EPO responses were expressed as functions of renal venous[Formula: see text] , the two strains appeared to lie on the same dose-response curves, but the responses of H rats were shifted along the curve toward more hypoxic values. We conclude that H rats have significantly greater polycythemia secondary to poorer renal tissue oxygenation, but the stimulus-response characteristics governing EPO gene expression and EPO production do not seem to differ between M and H rats. Finally, the regulation of EPO levels during hypoxia occurs primarily at the transcriptional level.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1998.84.4.1242
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 3
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    Online Resource
    Ventilatory and hematopoietic responses to chronic hypoxia in two rat strains
    American Physiological Society ; 1992
    In:  Journal of Applied Physiology Vol. 72, No. 6 ( 1992-06-01), p. 2354-2363
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 72, No. 6 ( 1992-06-01), p. 2354-2363
    Abstract: Hilltop (H) and Madison (M) strains of Sprague-Dawley rats exhibit strikingly different susceptibilities to the effects of chronic altitude exposure. The H rats develop greater polycythemia, hypoxemia, and pulmonary hypertension. We studied ventilation, pulmonary gas exchange, tissue oxygenation, and hematologic adaptations in the two rat strains during a 50-day exposure to a simulated altitude (HA) of 5,500 m (18,000 ft). There were no strain differences among the variables we studied under sea level (SL) conditions. Within the first 14 days of hypoxic exposure, the only significant strain differences were that erythropoietin (EPO) rose much higher and erythroid activity was greater in the H rats, even though arterial Po2 and PCo2 (Pao2 and PaCo2, respectively), renal venous PO2 (Prvo2), and ventilation (VE) were equivalent in the two strains during this time. By day 14 at HA, the H rats had significantly higher erythroid activity, hematocrit (Hct), and EPO levels, significantly lower PaO2 and PrvO2, but equivalent VE and PaCO2. These changes persisted for the remainder of the exposure, except that the Hct continued to rise and the increase was greater in H rats. Despite the greater O2-carrying capacity of H rats in the later stages of hypoxic exposure, PaO2 and PrvO2 were significantly lower in H rats. There were no strain differences at either SL or HA in ventilatory responses to hypercapnia or hypoxia, in blood O2 affinity or 2,3-diphosphoglycerate, in extrarenal production of EPO, or in EPO clearance. We conclude that early in the hypoxic exposure the H rats produce more EPO at apparently equivalent levels of hypoxia, and this is the first step in the pathogenesis of the maladaptation to HA manifest by H rats. We find no consistent evidence that differences in VE contribute to the variable susceptibility to hypoxia in the two rat strains.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1992.72.6.2354
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    Online Resource
    Online Resource
    Role of the spleen in the exaggerated polycythemic response to hypoxia in chronic mountain sickness in rats
    American Physiological Society ; 1999
    In:  Journal of Applied Physiology Vol. 87, No. 5 ( 1999-11-01), p. 1901-1908
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 87, No. 5 ( 1999-11-01), p. 1901-1908
    Abstract: In a rat model of chronic mountain sickness, the excessive polycythemic response to hypoxic exposure is associated with profound splenic erythropoiesis. We studied the uptake and distribution of radioactive iron and red blood cell (RBC) morphology in intact and splenectomized rats over a 30-day hypoxic exposure. Retention of 59 Fe in the plasma was correlated with 59 Fe uptake by both spleen and marrow and the appearance of 59 Fe-labeled RBCs in the blood. 59 Fe uptake in both the spleen and the marrow paralleled the production of nucleated RBCs. Splenic 59 Fe uptake was ∼10% of the total marrow uptake under normoxic conditions but increased to 60% of the total marrow uptake during hypoxic exposure. Peak splenic 59 Fe uptake and splenomegaly occurred at the most intense phase of erythropoiesis and coincided with the rapid appearance of 59 Fe-labeled RBCs in the blood. The bone marrow remains the most important erythropoietic organ under both resting and stimulated states, but inordinate splenic erythropoiesis in this rat strain accounts in large measure for the excessive polycythemia during the development of chronic mountain sickness in chronic hypoxia.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1999.87.5.1901
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
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  • 5
    Online Resource
    Online Resource
    Role of sex hormones in development of chronic mountain sickness in rats
    American Physiological Society ; 1994
    In:  Journal of Applied Physiology Vol. 77, No. 1 ( 1994-07-01), p. 427-433
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 77, No. 1 ( 1994-07-01), p. 427-433
    Abstract: After chronic exposure to hypoxia, Hilltop Sprague-Dawley rats developed excessive polycythemia and severe pulmonary hypertension and right ventricular (RV) hypertrophy, signs consistent with human chronic mountain sickness; however, there were gender differences in the magnitude of the polycythemia and susceptibility to the fatal consequence of chronic mountain sickness. Orchiectomy and ovariectomy were performed to evaluate the role of sex hormones in the gender differences in these hypoxic responses. After 40 days of exposure to simulated high altitude (5,500 m; barometric pressure of 370 Torr and inspired Po2 of 73 Torr), both sham-gonadectomized male and female rats developed polycythemia and had increased RV peak systolic pressure and RV hypertrophy. The hematocrit was slightly but significantly higher in males than in females. Orchiectomy did not affect these hypoxic responses, although total ventricular weight was less in the castrated high-altitude rats. At high altitude, the mortality rates were 67% in the sham-operated male rats and 50% in the castrated animals. In contrast, ovariectomy aggravated the high-altitude-associated polycythemia and increased RV peak systolic pressure and RV weight compared with the sham-operated high-altitude female rats. Both sham-operated control and ovariectomized females suffered negligible mortality at high altitude. The present study demonstrated that 1) the male sex hormones play no role in the development of the excessive polycythemia, pulmonary hypertension, and RV hypertrophy during chronic hypoxic exposure or in the associated high mortality and 2) the female sex hormones suppressed both the polycythemic and cardiopulmonary responses in vivo during chronic hypoxic exposure.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1994.77.1.427
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
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    Online Resource
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