摘要
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。
Objectie To explore the mechanism of the effect of chronic intermittent hypoxia(CIH),an important pathophysiological state of sleep apnea syndrome(SAS),on cardioascular system. Methods Thirty male ICR mice were diided 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-1α) and inducible nitric oxide synthase(NOS-2) in the myocardial cells. Enzyme-linked immunosorbent assay(ELISA) was used to measure the plasma concentration of ascular endothelial growth factor(EGF) and endothelin-1(ET-1). Results The expression of HIF-1α 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-1α 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 EGF 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-1α and its target gene products EGF and ET-1,and therefore affects the cardioascular system.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
2005年第2期93-96,共4页
Chinese Journal of Tuberculosis and Respiratory Diseases
