Effects of intermittent hypoxia on pulmonary arterial pressure and right ventricular mass

Chronic continuous hypoxia causes pulmonary hypertension and cor pulmonale secondary to hypoxic pulmonary vasoconstriction and pulmonary vascular remodelling. These effects are manifestations of the chronic hypoxia of respiratory disease, and are associated with increased morbidity and mortality. Although controversial, there is some evidence that chronic hypercapnia accompanying the hypoxia may ameliorate these changes. Chronic intermittent hypoxia and hypoxia/hypercapnia are associated with sleep-disordered breathing. There is controversy concerning the association of sleep apnoea and pulmonary hypertension and cor pulmonale. Some studies showed that nocturnal intermittent hypoxia must be accompanied by daytime continuous hypoxia for pulmonary arterial hypertension and cor pulmonale to be manifest whereas other studies showed that isolated nocturnal intermittent hypoxia with daytime normoxia was sufficient to produce these changes. In recent years, the effects on pulmonary arterial pressure and right ventricular mass of chronic intermittent hypoxia and asphyxia interspersed with prolonged periods of normoxia have been studied in animals. Chronic intermittent hypoxia increases right ventricular mass and/or pulmonary arterial pressure in rats and mice and chronic intermittent asphyxia increases right ventricular mass and pulmonary arterial pressure in rats in the absence of periods of continuous hypoxia. However, the inconsistency of the reports of the association of sleep apnoea and pulmonary hypertension and cor pulmonale and the poor correlation between these effects and sleep apnoea severity suggest that further work is required to elucidate the mechanisms that underlie the differences between the findings in animals and the human condition. Some of the mechanisms that may contribute to these discrepancies are discussed