Treatment of obstructive sleep apnoea leads to enhanced pulmonary vascular nitric oxide release

BackgroundObstructive sleep apnoea (OSA) is associated with pulmonary hypertension, however neither the pathogenesis of pulmonary vascular disease nor the effect of successful treatment of OSA on pulmonary vascular physiology has been characterised.MethodsSeven subjects aged 52 (range 36–63) years with moderate to severe obstructive sleep apnoea (apnoea–hypopnoea index > 15/h) had detailed pulmonary vascular reactivity studies, before and after 3 months of successful treatment with nasal continuous positive airways pressure (CPAP). On both occasions, we measured pulmonary pressure, flow velocity, flow and resistance, at baseline and in response to acetylcholine (an endothelium-dependent dilator), sodium nitroprusside (an endothelium-independent dilator), l-NMMA (an antagonist of nitric oxide synthesis) and l-Arginine (the substrate of nitric oxide).ResultsAt baseline, pulmonary flow increased in response to acetylcholine and nitroprusside and fell in response to l-NMMA. Following CPAP treatment, the decrease in flow to l-NMMA was significantly greater (to 62 ± 6% of control value vs 85 ± 6% of pre-treatment; p = 0.01), consistent with enhanced basal release of nitric oxide. The acetylcholine response tended to be greater after treatment (174 ± 26% of control vs 147 ± 12% of pre-CPAP, p = 0.22), however the nitroprusside response was unchanged.ConclusionSuccessful treatment of obstructive sleep apnoeic episodes in sleep results in enhanced nitric oxide release by the pulmonary microvascular circulation.