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

Hung-Yuan Cheng,Peter A Robbins,Quentin P P Croft,Keith L Dorrington,Matthew C Frise,Nick P Talbot,Nayia Petousi

doi:10.14814/phy2.13396

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.

Highlights

The human pulmonary circulation responds to alveolar hypoxia with an abrupt acute vasoconstriction occurring over a few (~5) minutes
The PETCO2 of each volunteer remained fairly constant during 8 h; there was a slight fluctuation during sustained hyperoxia
There was a significant difference between the hyperoxia exposure and the euoxia exposure in the values of SpO2 (Hyperoxia: 98.1 Æ 0.4%; Control: 96.8 Æ 0.3%, P = 0.016) (Fig. 3E)

Summary

Introduction

The human pulmonary circulation responds to alveolar hypoxia with an abrupt acute vasoconstriction occurring over a few (~5) minutes. If the hypoxia is maintained, this constriction begins to intensify after about 40 min (Talbot et al 2005), and continues to increase over the periods of 2–8 h that have been studied in various laboratory protocols (Dorrington et al 1997; Balanos et al 2002; Talbot et al 2014) This increasing vasoconstriction in the presence of a constant sustained hypoxic stimulus can be thought of as ‘pulmonary vascular acclimatization’ to hypoxia by analogy with the human ventilatory acclimatization to hypoxia that follows a similar time course. The question of whether the oxygen sensing of the pulmonary vasculature and that of the ventilatory control system share similarities in the manner in which they generate their respective acclimatizations to hypoxia continues to receive attention.

Methods

Results

Conclusion