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背景:降钙素基因相关肽可减轻心肌缺血再灌注损伤。肾上腺髓质素与降钙素基因相关肽有一定的同源性,因此,一些研究推测肾上腺髓质素也可能对心肌有保护作用。目的:探讨肾上腺髓质素对缺血再灌注大鼠心肌组织血管细胞黏附分子1表达的抑制及其对心肌缺血的保护作用。设计:实验对象为SD大鼠心脏缺血再灌注模型,完全随机分组,随机设计。材料:本实验于2003-12/2004-05在咸宁学院医学院实验动物中心完成。实验选用健康雄性SD大鼠24只。方法:24只雄性SD大鼠心脏制成离体心脏缺血再灌注模型,随机分为对照组和肾上腺髓质素1-50(1×10-9),(1×10-8),(1×10-7)mol/L组。心脏缺血60min,对照组用氧合KHB液再灌注60min,其他3组分别用氧合KHB液加肾上腺髓质素1-50(1×10-9),(1×10-8),(1×10-7)mol/L再灌注15min,再用KHB液灌注45min。收集冠状动脉流出液,检测肌酸激酶同工酶含量。留取左室心尖部心肌进行总RNA提取,采用RT-PCR法测定血管细胞黏附分子1mRNA的表达。主要观察指标:对照组及不同浓度肾上腺髓质素1-50组心肌组织VCAM-1mRNA的表达。结果:电泳后,各组在194bp处均可见一明显的扩增条带,此为甘油醛-3-磷酸脱氢酶mRNA扩增片段,各组间甘油醛-3-磷酸脱氢酶mRNA的表达基本一致。对照组、肾上腺髓质素1-50(1×10-9)mol/L组在334bp处可见亮度强、边界明显清楚的条带为血管细胞黏附分子1mRNA扩增片段。肾上腺髓质素1-50(1×10-8)mol/L组血管细胞黏附分子1mRNA扩增条带亮度明显减弱。肾上腺髓质素1-50(1×10-7)mol/L组仅为亮度微弱且模糊的扩增条带。肾上腺髓质素1-50(1×10-8),(1×10-7)mol/L组扩增的血管细胞黏附分子1mRNA与甘油醛-3-磷酸脱氢酶mRNA的灰度值比值(0.6±0.31,0.5±0.36)明显低于对照组(1.2±0.52)(P<0.05)。结论:心肌缺血再灌注时,肾上腺髓质素1-50可呈浓度依赖性地抑制心肌组织血管细胞黏附分子-1mRNA的表达。
BACKGROUND: Calcitonin gene-related peptide can reduce myocardial ischemia-reperfusion injury. Adrenomedullin and calcitonin gene-related peptide has some homology, therefore, some studies speculated that adrenomedullin may also have a protective effect on the myocardium. Objective: To investigate the effects of adrenomedullin on the expression of vascular cell adhesion molecule-1 (ICAM-1) and its protective effect on myocardial ischemia in myocardial ischemia-reperfusion rats. Design: The experimental rat model of myocardial ischemia / reperfusion was randomly divided into two groups: randomized design. MATERIALS: The experiment was performed at Experimental Animal Center of Xianning Medical College from December 2003 to May 2004. Twenty-four healthy male SD rats were selected for experiment. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into control and adrenomedullin 1-50 (1 × 10-9), (1 × 10-8), ( 1 × 10-7) mol / L group. The rats in the control group were reperfused with oxygenated KHB solution for 60 min. The other three groups were treated with oxygenated KHB solution and adrenomedullin 1-50 (1 × 10-9), (1 × 10-8), ( 1 × 10-7) mol / L for 15 min, followed by perfusion with KHB solution for 45 min. Coronary flow was collected and creatine kinase isoenzyme content was measured. Left ventricular apical myocardium was collected for total RNA extraction, and the expression of vascular cell adhesion molecule-1 mRNA was determined by RT-PCR. MAIN OUTCOME MEASURES: Expression of VCAM-1 mRNA in myocardium of control group and different concentrations of adrenomedullin 1-50 group. Results: After electrophoresis, a significant amplification band was observed at 194bp in each group, which was a fragment of the mRNA of glyceraldehyde-3-phosphate dehydrogenase. The mRNA of glyceraldehyde-3-phosphate dehydrogenase The expression is basically the same. In the control group, a band of 1mRNA of vascular cell adhesion molecule was clearly observed at 334bp in 1-50 (1 × 10-9) mol / L adrenomedullin group. Adrenomedullin 1-50 (1 × 10-8) mol / L group of vascular cell adhesion molecule 1mRNA amplification bands decreased significantly. Adrenomedullin 1-50 (1 × 10-7) mol / L group was only a weak and fuzzy amplified bands. The ratio of gray value of vascular cell adhesion molecule 1 mRNA and glyceraldehyde-3-phosphate dehydrogenase mRNA in adrenomedullin 1-50 (1 × 10-8), (1 × 10-7) mol / L group (0.6 ± 0.31,0.5 ± 0.36) was significantly lower than that of the control group (1.2 ± 0.52) (P <0.05). Conclusion: Adrenomedullin 1-50 can inhibit the expression of vascular cell adhesion molecule-1 mRNA in myocardial tissue in a concentration-dependent manner during myocardial ischemia-reperfusion.