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Human hypoxic pulmonary vasoconstriction is unaltered by 8 h of preceding isocapnic hyperoxia

Exposure to sustained hypoxia of 8 h duration increases the sensitivity of the pulmonary vasculature to acute hypoxia, but it is not known whether exposure to sustained hyperoxia affects human pulmonary vascular control. We hypothesized that exposure to 8 h of hyperoxia would diminish the hypoxic pu...

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Detalles Bibliográficos
Autores principales: Cheng, Hung‐Yuan, Croft, Quentin P. P., Frise, Matthew C., Talbot, Nick P., Petousi, Nayia, Robbins, Peter A., Dorrington, Keith L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599860/
https://www.ncbi.nlm.nih.gov/pubmed/28899910
http://dx.doi.org/10.14814/phy2.13396
Descripción
Sumario:Exposure to sustained hypoxia of 8 h duration increases the sensitivity of the pulmonary vasculature to acute hypoxia, but it is not known whether exposure to sustained hyperoxia affects human pulmonary vascular control. We hypothesized that exposure to 8 h of hyperoxia would diminish the hypoxic pulmonary vasoconstriction (HPV) that occurs in response to a brief exposure to hypoxia. Eleven healthy volunteers were studied in a crossover protocol with randomization of order. Each volunteer was exposed to acute isocapnic hypoxia (end‐tidal [Formula: see text]  = 50 mmHg for 10 min) before and after 8 h of hyperoxia (end‐tidal [Formula: see text]  = 420 mmHg) or euoxia (end‐tidal [Formula: see text]  = 100 mmHg). After at least 3 days, each volunteer returned and was exposed to the other condition. Systolic pulmonary artery pressure (an index of HPV) and cardiac output were measured, using Doppler echocardiography. Eight hours of hyperoxia had no effect on HPV or the response of cardiac output to acute hypoxia.