[Effect of chronic intermittent hypoxia on hypoxia inducible factor-1alpha in mice]

To explore the mechanism of the effect of chronic intermittent hypoxia (CIH), an important pathophysiological state of sleep apnea syndrome (SAS), on cardiovascular system.

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).

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).

CIH enhances the expression of HIF-1alpha and its target gene products VEGF and ET-1, and therefore affects the cardiovascular system.