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目的 探索睡眠呼吸暂停综合征(SAS)的慢性间断性缺氧(CIH)对心血管损害的可能机制。方法 制作CIH小鼠模型。将30只ICR小鼠均分为实验组、空气模拟对照组及空白对照组。免疫组织化学方法检测实验小鼠心肌细胞缺氧诱导因子1α(HIF1α)及诱导型一氧化氮合成酶(NOS2)的表达。酶联免疫吸附测定(ELISA)方法检测小鼠血浆血管内皮生长因子(VEGF)及内皮素1(ET1)的浓度。结果 实验组心肌细胞HIF1α表达高于空白对照组(t=354,P<005)及空气模拟对照组(t=292,P<005);空白对照组HIF1α表达与空气模拟对照组比较差异无统计学意义(P>005)。实验组血浆VEGF浓度[(957±141)ng/ml]高于空白对照组[(810±062)ng/ml,q=427,P<005]及空气模拟对照组[(832±099)ng/ml,q=364,P<005];空白对照组血浆VEGF浓度与空气模拟对照组比较差异无统计学意义(P>005)。实验组血浆ET1浓度[(331±081)ng/ml]高于空白对照组[(250±072)ng/ml,q=364,P<005];空气模拟对照组血浆ET1浓度[(269±043)ng/ml]与实验组及空白对照组[(331±081)、(250±072)ng/ml]比较差异均无统计学意义(P均>005)。小鼠心肌细胞NOS2表达在各组间比较差异均无统计学意义(P均>005)。结论 CIH可引起小鼠HIF1α表达增加,并可促进HIF1α目的基因产物VEGF、ET1的表达。这可能
Objective To explore the possible mechanism of chronic intermittent hypoxia (CIH) in patients with sleep apnea syndrome (SAS) on cardiovascular damage. Methods CIH mouse model was made. Thirty ICR mice were divided into experimental group, air control group and blank control group. Immunohistochemistry was used to detect the expression of hypoxia inducible factor 1α (HIF1α) and inducible nitric oxide synthase (NOS2) in experimental mouse cardiomyocytes. The concentrations of vascular endothelial growth factor (VEGF) and endothelin 1 (ET1) in mice were detected by enzyme-linked immunosorbent assay (ELISA). Results The expression of HIF1α in the experimental group was higher than that in the blank control group (t = 354, P <005) and the air control group (t = 292, Significance (P> 005). Plasma VEGF concentration in the experimental group [(957 ± 141) ng / ml] was significantly higher than that in the blank control group [(810 ± 062) ng / ml, q = 427, P < / ml, q = 364, P <005]. There was no significant difference in plasma VEGF concentration between the blank control group and the air control group (P> 005). The ET1 concentration in the experimental group was significantly higher than that in the blank control group [(331 ± 081) ng / ml [(250 ± 072) ng / ml, q = 364, P < 043) ng / ml] was not significantly different from that of the experimental group and the blank control group [(331 ± 081), (250 ± 072) ng / ml] (all P> The expression of NOS2 in mouse cardiomyocytes was not significantly different between the groups (P> 005). Conclusion CIH can increase the expression of HIF1α in mice and promote the expression of VEGF and ET1 in HIF1α gene. This may