Abstract
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 PO2 = 50 mmHg for 10 min) before and after 8 h of hyperoxia (end-tidal PO2 = 420 mmHg) or euoxia (end-tidal PO2 = 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.
| Original language | English |
|---|---|
| Article number | e13396 |
| Number of pages | 9 |
| Journal | Physiological Reports |
| Volume | 5 |
| Issue number | 17 |
| Early online date | 12 Sept 2017 |
| DOIs | |
| Publication status | Published - 12 Sept 2017 |
Bibliographical note
Funding Information:This research was funded by the Dunhill Medical Trust R178/1110.
Publisher Copyright:
© 2017 The Authors.
Keywords
- Cardiac output
- human
- hyperoxia
- pulmonary circulation
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