原发性高血压患者血清Fractalkine水平与血管内皮功能损伤的相关性研究

目的研究原发性高血压患者Fractalkine(FKN)与血管内皮功能的相关性。方法纳入50例原发性高血压患者作为高血压组,50例健康体检者为对照组。使用酶联免疫吸附法(ELISA)测定血清FKN水平,使用高效液相色谱法测定血浆非对称性二甲基精氨酸(ADMA)水平,硝酸还原酶法测定血清一氧化氮NO水平。使用高分辨超声检测肱动脉血流介导的内皮依赖性血管舒张功能(FMD)及非内皮依赖性舒张功能(NMD)。38例原发性高血压患者(剔除12例)接受3个月的规范降压治疗。比较治疗前后收缩压、FKN、ADMA、NO、FMD的变化水平,进一步分析FKN治疗前后变化量绝对值与收缩压、ADMA、NO、FMD变化量绝对值的相关性。结果与对照组比较,高血压组的血清FKN、血浆ADMA水平升高(P<0.05),FMD、血清NO水平降低(P<0.05)。FKN与ADMA、收缩压、舒张压呈正相关(r=0.785、0.730和0.785,均P=0.000),与NO、FMD呈负相关(r=-0.800和-0.783,均P=0.000)。经过3个月的降压治疗,发现收缩压、舒张压、FKN、ADMA比治疗前降低,NO、FMD比治疗前升高。其中FKN治疗变化绝对值(△FKN)与△收缩压、△舒张压、△FMD、△ADMA、△NO呈正相关(r=0.720、0.405、0.707、0.687和0.726,P=0.000、0.012、0.001、0.032和0.001)。结论原发性高血压患者血清FKN水平的升高与血管内皮功能的损伤可能有关。降压治疗可改善原发性高血压患者的内皮功能,降低血清中的FKN水平。

Comparative analysis of different cyclosporine A doses on protection after myocardial ischemia/reperfusion injury in rat

Objective:To investigate the protective effect of different cyclosporin A(CsA)doses on myocardial ischemia/reperfusion injury in rat models.Methods:A rat model of myocardial ischemia/reperfusion injury was established in vivo and the rats were randomly divided into four groups:placebo(PBS;T1),low-dose(CsA dose:1.0 mg/kg:T2),medium-dose(CsA dose:2.5 mg/kg:T3),and high-dose(CsA dose:5.0 mg/kg;T4)groups.Heart function indexes were monitored at different time points,the extent of myocardial infarction was assessed by Evans Blue-TTC staining,and creatine kinase MB mass and cardiac troponin 1 values were measured by biochemical assays.Results:Compared with the T1 and T2 groups,both the creatine kinase MB mass and cardiac troponin 1 were significantly lower in the T3 and T4 groups(P<0.05).The mean arterial pressure(MAP)and left ventricular systolic pressure(LVSP)decreased sequentially in each group,with the extending reperfusion time.Significant decreases in LVSP and MAP were observed in the T3 and T4 groups as compared to the T1 and T2 group(P<0.05)and the T2 group showed a significantly lower LVSP and MAP decline than the T1 group(P<0.05).Compared with the Tl group,the rats from the T2.T3,and T4 groups suffered from a significantly lower extent of myocardial infarction(P<0.05).Also,the a animals in the T3 and T4 groups had a significantly smaller extent of myocardial infarction than those in the T2 group(P<0.05).Conclusions:Various CsA doses exert different degrees of protection against ischemia/reperfusion injury,and this protective effect peaks at approximately 2.5 mg/kg in rat models.

Effects of hypokalemia on transmural dispersion of ventricular repolarization in left ventricular myocardium

Objective:To observe effects of hypokalemia on transmural heterogeneity of ventricular repolarization in left ventricular myocardium of rabbit,and explore the role of hypokalemia in malignant ventricular arrhythmia（MVA）.Methods:A total of 20 rabbits were randomly divided into control group and hypokalemic group.Isolated hearts in the control group were simply perfused with modified Tyrode’s solution,and were perfused with hypokalemic Tyrode’s solution in hypokalemic group.Ventricular fibrillation threshold（VFT）,90%monophasic action potential repolarization duration(APD90) of subepicardial,midmyocardial and subendocardial myocardium,transmural dispersion of repolarization（TDR） and Cx43 protein expression in three layers of myocardium were measured in both groups.Results:VFT in the control group and the hypokalemic group were（13.40±2.95） V,and（7.00±1.49） V,respectively.There was a significant difference between two groups（P【0.01）.APD90 of three myocardial layers in the hypokalemic group were significantly prolonged than those in the control group（/’【0.01）.△APD90in the hypokalemic group and the control group were（38.10±10\29） ms and（23.7015.68） ms,and TDR were（52.90r 14.55） ms and（36.10±12.44） ms,respectively.△APD90 and TDR in the hypokalemic group were significantly higher than those in the control group(P【0.05|,and the increase in△APD90 of midmyocardium was more significant in the hypokalemic group.Cx43 protein expression of all three myocardial layers were decreased significantly in the hypokalemic group（P【0.01）, and△APD90 was significantly increased {P【0.05).Reduction of Cx43 protein expression was more significant in the midmyocardium.Conclusions:Hypokalemic can increase transmural heterogeneity of Cx43 expression and repolarization in left ventricular myocardium of rabbit,and decrease VFT and can induce MVA more easily.

Effects of Ang Ⅱ perfusion on transmural heterogeneous of Cx43 in acute myocardial ischemia reperfusion

Objective:To observe the effects of angiotensin Ⅱ(Ang Ⅱ) pefusion on transmural heterogeneity of Cx43 expression in the rabbit model with acute myocardial ischemia reperfusion(MIR),and investigate the role of rennin-angiotensin system in malignant ventricular arrhythmia induced by MIR.Methods:Twenty rabbits were randomly divided into MIR group(n=10) and Ang Ⅱ group(n=10).MIR model was produced with traditional ligation and opening of the anterior descending coronary artery in all animal.The hearts in vitro in the MIR group and the Ang Ⅱ group were perfused with simply improved Tyrode's solution and containing Ang Ⅱ Tyrode's solution respectively.90%monophasic action potential repolarization duration,transmural dispersion of repolarization.Cx43 protein(Cx43-pro) and mRNA(Cx43-Cq) expression in subepicardial,midmyocardial and subendocardial myocardium were measured in both groups.The greatest differences of Cx43-pro and Cx43-Cq among three myocardial layers were calculated and shown with △Cx43-pro and △Cx43-Cq respectively.Results:After Ang Ⅱ perfusion,90%monophasic action potential repolarization duration among three myocardial layer were significantly prolonged(P < 0.05 and P < 0.01),and transmural dispersion of repolarization also significantly increased compared with the MIR group(P < 0.05).Compare with the MIR group,three myocardial Cx43-pro and Cx43-Cq expression in the Ang Ⅱ group were significantly decreased(P < 0.05 and P < 0.01).but△Cx43-pro and △Cx43-Cq were significant increased.Conclusions:Renin-angiotensin system increases transmural heterogeneity of Cx43 expression in the rabbit model with MIR by Ang Ⅱ,and enlarge transmural dispersion of repolarization among three myocardial layers of left ventricular which induces malignant ventricular arrhythmia.