摘要
目的 :观察心肌缺血对血浆及心肌组织内皮素 (ET)浓度影响的量效及时效改变 ,并初步探讨其机制。方法 :用不同剂量的垂体后叶素 (Pit)诱发大鼠在体心肌缺血并观察了相同剂量Pit作用下的不同时点的大鼠心肌组织及血浆的ET浓度的变化 ,然后做心肌ET - 1的免疫组化及基因表达。结果 :随着Pit剂量的加大 ,血浆及心肌组织ET浓度逐渐升高 ,当Pit剂量升至 15U/kg体重时 ,其ET浓度高于对照组 (P <0 0 5 ) ;Pit注射后 1hET浓度升至高峰 ,当缺血时间大于 1h后 ,ET浓度有所回降 ,但仍明显高于对照组。免疫组化显示ET - 1主要定位在心肌细胞和血管内皮细胞 ,缺血组心肌ET - 1染色灰度值明显低于对照组 (P <0 0 1) ;RT -PCR结果显示缺血组PCR产物条带灰度值显著高于对照组 (P <0 0 1)。结论 :垂体后叶素性心肌缺血可引起血浆及心肌ET浓度的升高并呈现一定的量效及时效关系 ,这可能与缺血刺激心肌ET - 1基因的表达及蛋白合成有关。
AIM: To study dose-effect and time-effect changes of endothelin (ET) in myocardium and plasma during myocardial ischemia and its mechanism. METHODS:After inducing myocardial ischemia of rats in vivo with different dose of pituitrin(Pit) and the optimal dosage in the Pit at different time point, ET concentration in the myocardium and plasma was measured.Moreover, immunohistochemical study and RT-PCR were also applied in this study. RESULTS:ET concentration in myocardium increased gradually with the increase of Pit dose. ET concentration elevated significantly ( P< 0.05) when the dosage of Pit was 15 U/kg body weight for one hour after administration of Pit. The tendency of change of plasma ET was similar with that of ischemic mycardium. When ischemic time exceed 1h ,ET concentration began to decrease but still above the control level. Immunohistochemical study showed that vascular endothelial cell and cardiac myocytes appeared to be the principal ET-1 synthetic sites, also, the ET level in ischemia group was more markedly increased than that of control group ( P <0.01) The results of RT-PCR showed that ET mRNA in ischemia group was more than that of control group ( P <0.01). CONCLUSION: Endothelin expression increased significantly during myocardial ischemia.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第5期501-504,T001,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (No .39770 936 )
广东省自然科学基金资助项目 (No.96 0 113)
