Treatment of Obstructive Sleep Apnea-Hypopnea Syndrome With a Mandible Advanced Device Increases Nitric Oxide Release and Ameliorates Pulmonary Hypertension in Rabbits.

PURPOSE: To investigate the effects of mandible advanced device (MAD) therapy for obstructive sleep apnea-hypopnea syndrome (OSAHS) on nitric oxide (NO) release and changes in pulmonary artery pressure and structure.

METHODS

Thirty male New Zealand white rabbits were randomly divided into OSAHS, MAD, and control groups (n = 10 per group). The soft palate of rabbits in the OSAHS and MAD groups was injected with hydrophilic polyacrylamide gel to induce OSAHS. The MAD group wore a MAD, and the control group was not treated. Cone-beam computed tomography scans and polysomnography recordings were performed to confirm successful model establishment. All rabbits slept in a supine position for 4 to 6 hours daily and were observed for 8 consecutive weeks. The pulmonary artery pressure was measured by right heart catheterization. Pulmonary artery morphometry was analyzed by hematoxylin and eosin staining. NO levels in plasma and lung homogenate supernatants were detected by Griess reaction assay kits.

RESULTS

The OSAHS group exhibited higher pulmonary artery pressure (57.74 ± 1.79 mm Hg) than the MAD (19.99 ± 2.04 mm Hg) and control (14.49 ± 0.54 mm Hg) groups. The media thickness percentage of the pulmonary artery was higher in the OSAHS group (46.89 ± 2.72%) than the control group (15.87 ± 1.18%) and was markedly reduced by MAD (21.64 ± 1.45%). Blood oxygen saturation was positively correlated with the NO concentration in both the lung and plasma, and the NO concentration was negatively correlated with the media thickness percentage and media section percentage.

CONCLUSIONS

OSAHS induced a decrease in NO and pulmonary hypertension, which was relieved by MAD therapy.