ABSTRACT
OBJECTIVE: To explore the mechanism of the effect of chronic intermittent hypoxia (CIH), an important pathophysiological state of sleep apnea syndrome (SAS), on cardiovascular system. METHODS: Thirty male ICR mice were divided into three groups: an experimental group, an air mimic control group and a blank control group. Immunohistochemistry was used to examine the expression of hypoxia inducible factor-1alpha (HIF-1alpha) and inducible nitric oxide synthase (NOS-2) in the myocardial cells. Enzyme-linked immunosorbent assay (ELISA) was used to measure the plasma concentration of vascular endothelial growth factor (VEGF) and endothelin-1 (ET-1). RESULTS: The expression of HIF-1alpha in myocardial cells of the experimental group significantly increased compared with that of the air mimic control group (t = 3.54, P < 0.05), and that of the blank control group (t = 2.92, P < 0.05). The expression of HIF-1alpha in myocardial cells of the air mimic control group was not significantly different from that of the blank control group (P > 0.05). The plasma concentration of VEGF of the experimental group [(9.57 +/- 1.41) ng/ml] was significantly higher than that of the blank control group [(8.10 +/- 0.62) ng/ml, q = 4.27, P < 0.05], and that of the air mimic control group [(8.32 +/- 0.99) ng/ml, q = 3.64, P < 0.05]. While the plasma concentration of ET-1 of the experimental group [(3.31 +/- 0.81) ng/ml] was significantly higher than that of the blank control group [(2.50 +/- 0.72) ng/ml, q = 3.64, P < 0.05], it was not significantly different from that of the air mimic control group [(2.69 +/- 0.43) ng/ml, P > 0.05]. There was no significant difference between the expression of NOS-2 in myocardial cells of all groups (P > 0.05). CONCLUSION: CIH enhances the expression of HIF-1alpha and its target gene products VEGF and ET-1, and therefore affects the cardiovascular system.