Open AccessHuman hypoxic pulmonary vasoconstriction is unaltered by 8 h of preceding isocapnic hyperoxia
Author(s) -
Cheng HungYuan,
Croft Quentin P. P.,
Frise Matthew C.,
Talbot Nick P.,
Petousi Nayia,
Robbins Peter A.,
Dorrington Keith L.
Publication year - 2017
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13396
Subject(s) - hyperoxia , hypoxic pulmonary vasoconstriction , hypoxia (environmental) , medicine , vasoconstriction , anesthesia , cardiology , pulmonary artery , vascular resistance , lung , hemodynamics , oxygen , chemistry , organic chemistry
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 P O 2 = 50 mmHg for 10 min) before and after 8 h of hyperoxia (end‐tidal P O 2 = 420 mmHg) or euoxia (end‐tidal P O 2 = 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.