Protective effect of fosinopril sodium pretreatment combined with ischemic postconditioning on rat heart underwent myocardial ischemia/reperfusion injury
10.3760/cma.j.issn.0253-3758.2010.07.015
- VernacularTitle:福辛普利钠预处理结合缺血后适应对大鼠心肌缺血再灌注损伤的保护作用
- Author:
Da-Wu ZHANG
1
;
Lei ZHANG
;
Jian-Gang LIU
;
Cheng-Long WANG
;
Da-Zhuo SHI
;
Ke-Ji CHEN
Author Information
1. 中国中医研究院西苑医院
- Keywords:
Myocardial reperfusion injury;
Fosinopril;
Ischemic postconditioning
- From:
Chinese Journal of Cardiology
2010;38(7):633-637
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of fosinopril sodium pre-treatment combined with ischemic postconditioning on rat serum and myocardial oxidative stress and proinflammatory cytokines post ischemia/reperfusion. Methods Sixty Sprague-Dawley rats were randomly divided into sham group ( n = 15 ) , ischemia/reperfusion group ( 30 minutes in situ occlusion of the left anterior descending artery followed by 1 hour nitrotetrazolium blue chloride staining, SOD content was examined by colorimetric method, MDA content was detected using thiobarbituric acid method, serum levels of Interleukin-1α (IL-lα), Interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-α) were examined by radioimmunoassay, IL-lα, IL-6 and TNF-α levels of myocardial tissue were detected by ELISA. Results Compared with I/R group, myocardial enzymes and infarction size were significantly decreased ( P < 0. 05, P < 0.01) , serum SOD content was increased and MDA content was decreased (allP<0.01), serum and myocaidial levels of IL-1α, IL-6 and TNF-α were significantly reduced (P<0. 05,P<0.05, P<0.01) in IPoC group. Compared with IPoC group, fosinopril sodium pretreatment further reduced infarction size and myocardial enzyme CK-MB ( P < 0.05 ) , increased SOD content ( P < 0. 05 ) while reduced serum IL-6 and myocaidial tissue TNF-a (P <0. 05, P <0.01). Conclusion Pretreatment with fosinopril sodium enhanced the protective effect of IPoC on rat myocardium underwent I/R injury, possibly by reducing oxidative stress and early inflammatory reaction.
