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Título:
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Hypercapnic ventilatory response is decreased in a mouse model of excessive erythrocytosis
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Autores:
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Laouafa, Sofien ;
Elliot-Portal, Elizabeth ;
Revollo, Susana ;
Schneider-Gasser, Edith-M. ;
Joseph, Vincent ;
Voituron, Nicolas ;
Gassmann, Max ;
Soliz, Jorge
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Tipo de documento:
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texto impreso
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Editorial:
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American Physiological Society, 2019-02-06T14:45:36Z
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Nota general:
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info:eu-repo/semantics/restrictedAccess
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
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Idiomas:
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Inglés
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Palabras clave:
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Editados por otras instituciones
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Artículos
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Artículos en revistas indizadas
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Resumen:
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The impact of cerebral erythropoietin (Epo) in the regulation of the hypercapnic ventilatory response (HcVR) is controversial. While we reported that cerebral Epo does not affect the central chemosensitivity in C57Bl6 mice receiving an intracisternal injection of sEpoR (the endogenous antagonist of Epo), a recent study in transgenic mice with constitutive high levels of human Epo in brain and circulation (Tg6) and in brain only (Tg21), showed that Epo blunts the HcVR, maybe by interacting with central and peripheral chemoreceptors. High Epo serum levels in Tg6 mice lead to excessive erythrocytosis (hematocrit ~80-90%), the main symptom of chronic mountain sickness (CMS). These latter results support the hypothesis that reduced central chemosensitivity accounts for the hypoventilation observed in CMS patients. To solve this intriguing divergence, we reevaluate HcVR in Tg6 and Tg21 mouse lines, by assessing the metabolic rate [O consumption (V) and CO production (V)], a key factor modulating ventilation, the effect of which was not considered in the previous study. Our results showed that the decreased HcVR observed in Tg6 mice (~70% reduction;
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En línea:
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http://doi.org/10.1152/ajpregu.00226.2016
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