Objective: To investigate the mechanism of vascular endothelial cell injury in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS).
Methods: Peripheral blood samples were collected early in the morning from 20 normal persons, 21 patients with mild OSAHS, 24 patients with moderate OSAHS, and 20 patients with severe OSAHS according to the results of polysomnography (PSG). Mononuclear cells (MNCs) were isolated and co-cultured with human umbilical vein endothelial cells of the strain ECV304 for 48 h. The levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 in the supernatant were measured by ELISA, and the apoptosis rate and the protein expression level of Fas of the endothelial cells were detected by flow cytometry.
Results: The TNF-alpha level of the severe OSAHS group was (2.10 +/- 0.60) microg/L, significantly higher than those of the moderate OSAHS, mild OSAHS, and normal control groups [(1.40 +/- 0.50) microg/L, (1.20 +/- 0.30) microg/L, and (0.80 +/- 0.10) microg/L, F = 69.65, P < 0.01]. The IL-6 level of the severe OSAHS group was (64.80 +/- 9.90) microg/L, significantly higher than those of the moderate OSAHS, mild OSAHS, and normal control groups [(46.90 +/- 10.80) microg/L, (49.60 +/- 2.80) microg/L, and (23.50 +/- 6.50) microg/L, F = 182.83, P < 0.01]. The TNF-alpha and IL-6 levels of the severe OSAHS group were both significantly higher than those of the moderate and mild OSAHS groups (both P < 0.01). However, there was no significant differences in the TNF-alpha and IL-6 levels between the mild and moderate OSAHS groups (both P > 0.05). The apoptosis rates of endothelial cells in the severe and moderate OSAHS groups were 19.6% +/- 3.8% and 19.3% +/- 6.3% respectively, both significantly higher than those of the mild OSAHS and control groups (9.2% +/- 3.0% and 8.3% +/- 3.2% (both P < 0.01) whereas there were no significant differences between the mild OSAHS group and control group and between the moderate OSAHS group and severe group (both P > 0.05). There was no significant difference in the protein level of Fas expressed in the endothelial cells between the OSAHS patients and the controls (all P > 0.05). There was a significant positive correlation between the apoptosis rate of endothelial cells and AHI (r = 0.589 13, P = 0.0106), and a significant negative correlation between the apoptosis rate and the minimum oxygen saturation (r = -0.507 37, P < 0.0001).
Conclusion: MNCs may play an important role in vascular endothelial cell injury in the OSAHS patients, and may be associated closely with the severity of the OSAHS and night hypoxemia.