Effects of intermittent hypoxia on pulmonary haemodynamics

Abstract

Acute alveolar hypoxia is the most potent pulmonary vasoconstrictor. Chronic alveolar hypoxia results in remodeling of the pulmonary arterial tree leading to pulmonary hypertension, and cor pulmonale. Contrary to the well known effects of continuous alveolar hypoxia, the effects of intermittent hypoxia (IH) on pulmonary haemodynamics are not well established. The aim of this chapter is to analyze effects of chronic IH on pulmonary haemodynamics comparing the results of animal experiments to those of investigations in humans. In animal experiments even short hypoxic exposure, continuously or in short repeated episodes mimicking obstructive sleep apnoea/hypopnoea syndrome (OSAHS) leads to pulmonary artery remodelling and to pulmonary hypertension. Results of clinical investigations on effects of nocturnal IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary disease (COPD) are discordant. Earlier studies reported the development of mild pulmonary hypertension in the subjects with O2 desaturation during sleep, while more recent investigations did not confirm these findings. Alveolar IH developing during apnoeic episodes during sleep in patients with OSAHS is a disease-induced model to study its effects on pulmonary haemodynamics. In the majority of studies in patients with OSAHS, pulmonary arterial pressure remained within normal values. Pulmonary hypertension was found in patients with OSAHS accompanied by COPD and/or extreme obesity. People commuting between lowland and high altitude because of their employment, are also repeatedly exposed to IH. Results of clinical investigations suggest that IH did not lead to development of permanent pulmonary hypertension. The reasons for such discrepancies between effects of IH in animal models and in humans remain to be studied. © 2009 Nova Science Publishers, Inc. All rights reserved.