Objective.-Heart failure is a major and escalating public health problem. Recent studies have demonstrated that statins prevented chronic heart failure (CHF) in animal studies. However, it is unknown whether statins therapy initiated after left ventricular (LV) hypertrophy is evident can still effectively prevent CHF. This study tested the hypothesis that statins can prevent the transition of hypertrophy to heart failure. Methods and results.-The rats were studied at 6, 12, and 20 weeks after aortic stenosis (AS) operation. Some rats were given simvastatin (2.0mg kg-1 per day) from 13 weeks after AS operation for 8 weeks. Coarctation of aorta in rats resulted in compensatory LV hypertrophy (LVH), concomitant with an increase of superoxide levels and cardiomyocyte apoptosis in LV tissues at 12 weeks after AS operation. This was followed by CHF with a progressive increase in superoxide levels and cardiomyocyte apoptosis in LV tissues at 20 weeks after AS operation. Simvastatin treatment initiated from 13 weeks after AS operation significantly improved LV function and reduced superoxide levels and cardiomyocyte apoptosis in LV tissues. Pretreatment of simvastatin suppressed the hydrogen peroxide-induced apoptosis of cultured cardiomyocytes from neonatal rats. Conclusions. -These data indicate that long-term administration of simvastatin improved LV function and prevented the transition of hypertrophy to CHF. Inhibition of oxidative stress and cardiomyocyte apoptosis may contribute to the benefits of simvastatin treatment on heart of rats with AS.

Neuropeptide Y (NPY) has been shown to participate in cardiac hypertrophy. However, the mechanisms by which NPY induces cardiomyocyte hypertrophy are poorly understood. This study tested the hypothesis that NPY induces cardiomyocyte hypertrophy through Ca2+/CaM-dependent calcineurin (CaN) pathway in cultured neonatal rat cardiomyocytes. After 24-h treatment, NPY (100 nM) significantly increased 3H-leucine incorporation and c-Jun mRNA expression, concomitant with augment of CaN activity and protein level in cardiomyocytes compared to those cells without NPY treatment. The enhancement of 3H-leucine incorporation and c-Jun mRNA expression in cardiomyocytes treated with NPY were markedly inhibited by cyclosporine A (CsA), a selective inhibitor of CaN. We also investigated the effect of NPYon intracellular Ca2+ level in cardiomyocytes. There were no obvious changes in intracellular Ca2+ level of cytoplasm and nucleus in cardiomyocytes treated with NPY (100 nM) for 10 min. However, NPY significantly increased intracellular Ca2+ level of cytoplasm and nucleus in cardiomyocytes after 24-h treatment. The result suggested that NPY could induce hypertrophy of cardiomyocytes via Ca2+/CaMdependent CaN signal pathway. The enhancement of [Ca2+]i caused by NPY may activate CaN signal pathways to mediate cardiac hypertrophy.

利用当前医院改革发展之医院集团式经营模式。根据病人转诊需求。通过信患技术实现了转诊病人信息交换的目标。实际运行表明。系统的构思和设计菏台国情。为推进医疗改革提供了技术支持。

目的 检测犬心肺复苏后6h，肺组织TNF-a、IL-6浓度和肺中TNF-amRNA、IL6mRNA、IL-10-mRNA的表达变化，以探讨纳洛酮对肺组织中TNF-a、IL-6、IL-10含量的影响。方法 18只健康杂种犬。随机分成3组，空白组（n=6）：不诱发室颤。6h后取肺组织：对照组（n=6）：心跳骤停后予常规心肺复苏术，实验组（n=6）：心跳骤停后予常规心肺复苏术+纳洛酮。于复苏后6h取肺组织行TNF-a、IL-6浓度和肺TNF-a；mRNA、IL-6mRNA、IL10mRNA的表达的测定以及行肺形态学检查。结果 实验组TNF-a浓度明显低于对照组（P<0.01），实验组、对照组、空白组IL-6浓度无差别（P>0.05）。实验组IL-10mRNA的表达明显高于对照组（P<0.05），实验组和对照组的TNF-amRNA、IL-6mRNA的表达无差别（P>0.05）。实验组肺组织的病理损害低于对照组。结论 纳洛酮可减轻心跳骤停后肺组织的TNF-a的生成，使IL-10mRNA的表达增加，从而减轻心肺复苏后肺的再灌流损伤。

目的 探讨以HSP70作为神经肽Y（NPY）和losartan间在肾动脉血管平滑肌细胞（VSMC）增殖活动相互作用为信号，在高血压肾动脉重塑中的作用。方法 应用快速微量MTT比色法和荧光免疫组织化学定量技术，观察神经肽Y作用下肾动脉VSMC增殖活动中热休克蛋白（heatHSP）表达以及Losartan对NPY作用的干预作用。结果 神经肽Y刺激体外培养肾动脉平滑肌细胞的增殖度（吸光度A值为0.2626±0.0025）与细胞内因损伤产生的HSP70表达（A值为0.2440±0.0013）明显高于对照组（A值为0.2239±0.0010）（P<0.01）。losartan可降低NPY对肾动脉平滑肌细胞的增殖度（A值）的刺激作用，减少细胞内HSP70的表达。结论 神经肽Y可影响肾动脉平滑肌细胞增殖引起高血压，而HSP70表达水平是肾动脉平滑肌细胞增殖的重要信号。