中文摘要：

目的：研究人urotensinⅡ（human urotensin II,h UII）对大鼠心肌细胞缺氧-再给氧损伤的作用及机制。方法：将培养的新生大鼠心肌细胞缺氧3 h后再给氧3 h造成细胞缺氧再给氧损伤（A/R）模型,用台盼蓝染色和MTT染色法分别检测细胞存活率和细胞活性,测定细胞培养上清液中肌酸激酶（CK）和一氧化氮合酶（NOS）活性及一氧化氮（NO）和心肌肌钙蛋白I（c Tn I）含量,用激光共聚焦显微镜检测细胞内游离Ca^2＋荧光强度。结果：在1×10^-10.5～1×10^-9.5mol/L范围内,h UII明显地抑制A/R损伤引起的大鼠心肌细胞存活率和细胞活性的下降、CK活性和c Tn I含量的增高、NOS活性和NO含量的降低及心肌细胞内游离Ca^2＋含量的增高,但1×10^-9、1×10^-8.5、1×10^-8mol/L h UII却无上述抑制作用。结论：h UII在低浓度时,对大鼠心肌细胞缺氧性损伤有保护作用,其机制可能与促进NO合成和降低细胞内游离Ca^2＋有关。

英文摘要：

AIM： To study effect and mechanism of human urotensin II（ h UII） on primarily cultured rat myocardial cells subjected to anoxia-reoxygenation（ A / R） injury. METHODS： The cultured neonatal rat cardiomyocytes were subjected to 3 h of anoxia followed by 3 h of reoxygenation. Cell viability and cellular activity were measured by the Trypan blue staining assay and the MTT assay,respectively. Activities of creatine kinase（ CK） and nitric oxide synthase（ NOS） and contents of nitric oxide（ NO） and cardiac troponin I（ c Tn I） in the supernate culture fuid were determinated. The intracellular free calcium fluorescence intensity in the cultured at myocardial cells was monitored by laser scanning confocal microsope. RESULTS： In the range of 1 ×10^-10.5-1 × 10^-9.5mol / L,h UII significantly inhibited A / R injury-induced decreases of rat myocardial cell viability and cellular activity,increases of CK activity and c Tn I content,reductions of NOS activity and NO content and increase of myocardial free Ca^2＋ content. But 1 × 10^-9,1 × 10^-8.5and 1 × 10^-8mol / L h UII did not have above inhibitory effects. CONCLUSION： At lower concentration,h UII has protective effect on rat cardiomyocytes with anoxia and reoxygenation,which may relate to the promoting NO production and reducing intracellular free Ca^2＋ content.