摘要
目的 探讨肾上腺髓质素 (Adm1 5 0 )对缺血再灌注大鼠心肌组织血管细胞粘附分子 1(VCAM 1)表达的影响。方法 2 4只雄性SD大鼠 ,制作离体心脏缺血再灌注模型 ,并随机分为A、B、C、D4组 ,每组 6只。心脏缺血 6 0min ,A组用氧合K H液再灌注 6 0min ,B、C、D组用氧合K H液分别加入10 -9mol/L、10 -8mol/L、10 -7mol/L的Adm1 5 0再灌注 15min ,再用K H液灌注 45min。逆转录 -聚合酶链式反应 (RT PCR)法检测心肌组织VCAM 1mRNA表达 ,并测定磷酸肌酸激酶同工酶 (CK MB)释放。结果 Adm1 5 0抑制再灌注大鼠心肌组织VCAM 1表达的作用呈浓度依赖性。Adm1 5 0减少了再灌注末心肌组织CK MB漏出量 ,A组 ( 31 5± 3 3)U/L、B组 ( 2 9 7± 3 3)U/L、C组 ( 2 4 3± 3 0 )U/L、D组 ( 19 3± 3 2 )U/L ,C、D组与A组比较P <0 0 1。结论 心肌缺血再灌注时 ,Adm1 5 0通过抑制VCAM 1mRNA表达而产生心肌保护作用。
Objective: To investigate the effects of adrenomedullin1-50 (Adm1-50) on vascular cell adhesion molecule-1 (VCAM-1) expression in isolated rat heart. Methods: Twenty-four male Sprague-Dawley rat, weighting 300 to 350g, were randomly divided into A, B, C, D group (n=6 for each group). The isolated rat hearts were perfused in a Langendorff mode for 20 min and followed by 60 min of global ischemia. Then, all groups were reperfused with Kerbs-Henseleit bicarbonate for 60 min, but group B, C, D were perfused with buffer in the presence of Adm1-50 10-9mol/L, 10-8mol/L, and 10-7mol/L respectively for 15 min after the onset of reperfusion. The post-ischemic change of creatine kinase-isoenzyme (CK-MB) in coronary effluent and the expression of myocardial VCAM-1 mRNA were measured. Results: After I/R, Adm1-50 dose-dependently decreased the expression of VCAM-1 and the CK-MB activity, The ratio of VCAM-1/GAPDH mRNA were 1 20±0 52, 1 10±0 45, 0 60±0 31, 0 50±0 36 for group A, B, C, D, respectively (P<0 01, group C and D vs. group A). Conclusion: Adm1-50 may protected the myocardium from I/R injury by inhibiting the expression of VCAM-1.
出处
《中华胸心血管外科杂志》
CSCD
北大核心
2003年第2期103-105,共3页
Chinese Journal of Thoracic and Cardiovascular Surgery
关键词
心肌再灌注损伤
心肌缺血
血管细胞粘附分子
肾上腺髓质素
Myocardial reperfusion injury
Myocardial ischemic
Vascular cell adhesion molecules-1
Adrenomedullin
