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异丙肾上腺素诱导的急性心肌损伤大鼠一氧化氮系统的变化 被引量:4

Changes of nitric oxide system on isoproterenol-induced acute myocardial injury in rats
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摘要 目的建立异丙肾上腺素(ISO)诱导的急性心肌损伤大鼠模型,观察急性心肌损伤大鼠NO系统的变化。方法将SD大鼠随机分为两组,对照组和模型组。模型组连续3d皮下注射ISO(150mg·kg-1·d-1)。通过血清肌酸激酶(CK)和乳酸脱氢酶(LDH)的活性和Ⅱ导联心电图来判定心肌损伤与否。用荧光定量RT-PCR来分析三种一氧化氮(eNOS、nNOS、iNOS)以及肿瘤坏死因子-α(TNF-α)的mRNA转录水平。结果模型组血清CK、LDH的活性显著增加(P<0.001),ST段明显上抬。与正常组相比,模型组eNOS和nNOS的转录水平显著降低(P<0.001);而iNOS和TNF-α的转录水平显著升高(P<0.001)。结论ISO诱导的心肌损伤大鼠NO系统发生的主要变化为三种NOS转录水平的改变。 Objective To establish a rat model with acute myocardial injury induced by isoproterenol and to investigate the changes of nitric oxide system. Methods SD rats were randomly divided into ISO-group and control group. The acute myocardial injury was induced by subcutaneous injection of isoproterenol (150 mg·kg^-1·d^-1). Myocardial injury was investigated by serum CK and LDH activity and electrocardiography in lead Ⅱ. The mRNA level of three nitric oxide synthase isoforms (eNOS, nNOS, iNOS) and TNF-α were analyzed by real time RT-PCR. Results ST-segment elevation and increase of serum LDH and CK activity were detected in ISO group. The mRNA levels of both eNOS and nNOS significantly decreased compared with those in the control group. However, those of iNOS and TNF-α significantly increased, Conclusion There were significant changes in the mRNA levels of three NOS isoforms on acute myocardial injury in rats. It maybe closely correlated with the inflammation, which need further studies.
出处 《中国心血管病研究》 CAS 2006年第7期539-541,共3页 Chinese Journal of Cardiovascular Research
基金 香港赛马会慈善基金资助
关键词 异丙肾上腺素 心肌损伤 一氧化氮合酶 肿瘤坏死因子 Isoproterenol Heart injuries Nitric oxide synthase Tumor necrosis factor
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  • 1[1]Acikel M,Buyukokuroglu ME,Erdogan F,et al.Protective effects of dantrolene against myocardial injury induced by isoproterenol in rats:biochemical and histological findings.Inter J Cardiol,2005,98:389-394.
  • 2[2]Vimal V,Devaki T.Linear furanocoumarin protects rat myocardium against lipidperoxidation and membrane damage during experimental myocardial injury.Biomedi & Pharmacother,2004,58:393-400.
  • 3[3]Kupatt C,Hinkel R,Vachenauer R,et al..VEGF165 transfection decreases postischemic NF-(B-dependent myocardial reperfusion injury in vivo:role of eNOS phosphorylation.FASEB J,2003,17:705-707.
  • 4[4]Massion PB,Feron O,Dessy C,et al.Nitric oxide and cardiac function.Circ Res,2003,93:388-398.
  • 5[5]Grimm D,Elsner D,Schunkert H,et al.Development of heart failure following isoproterenol administration in the rat:role of the renin-angiotensin system,Cardiovasc Res,1998,37:91-100.
  • 6[6]Feron O,Dessy C,Opel DJ,et al.Modulation of the endothelial nitric-oxide synthase-caveolin interaction in cardiac myocytes:implications for the autonomic regulation of heart rate.J Biol Chem,1998,273:30249-30254.
  • 7[7]Ashley EA,Sears CE,Bryant SM,et al.Cardiac nitric oxide synthase 1 regulates basal and β-adrenergic contractility in murine ventricular myocytes.Circulation,2002,105:120-125.
  • 8[8]Takimoto Y,Aoyama T,Tanaka K,et al.Augmented expression of neuronal nitric oxide synthase in the atria parasympathetically decreases heart rate during acute myocardial infarction in rats.Circulation,2002,105:490-496.
  • 9[9]Yoshizumi M,Perrella MA,Burnett JC,et al.Tumor necrosis factor downregulates an endothelial nitric oxide synthase mRNA by shortening its half-life.Circ Res,1993,73:205-209.

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