目的:探讨坎地沙坦与依那普利联合应用对高血压合并左心室肥厚患者血压及左室重构的影响。方法:选择65例高血压合左心室肥厚患者为研究对象,随机分为2组,分别给予坎地沙坦和坎地沙坦与依那普利联合治疗,疗程共26周。采用彩色超声技术测定治疗前、后左心室肥厚的参数变化,并记录血压的变化。结果:坎地沙坦与依那普利联合应用能明显改善高血压患者左室舒张功能，逆转左室肥厚(Plt;005);坎地沙坦单用或与依那普利联合应用均能明显降低血压(Plt;005),但二者联合应用的降压效果与坎地沙坦单独应用的效果相比,差异没有显著性意义(Pgt;005)。 结论:坎地沙坦与依那普利联合应用具有较好的降压效果,并能明显阻断心室重构、改善心脏功能。
【摘要】 目的 探讨坎地沙坦干预后海仁藻酸（kainic acid，KA）致痫大鼠肾脏细胞外信号调节激酶（ERK1/2）的表达及其变化的机制。 方法 105只雄性Wistar大鼠随机分为3组:A1-5对照组、B1-5 致痫组、C1-5坎地沙坦组，每组各35只，1-5分别表示癫痫后0、2、6、12及24 h。采用立体定位仪下杏仁核内注射KA方法制备大鼠癫痫模型，于致痫后不同时程，进行灌流固定、肾脏组织的石蜡包埋、切片及免疫，组织化学染色，检测不同时程肾脏ERK1/2表达的灰度值。 结果 与对照组相比，致痫组及坎地沙坦组肾组织于致痫后2 h ERK1/2表达均开始增加（致痫后2 h ERK1/2，致癫组：20 229.18±2 067.27，坎地沙坦组：16 878.19±2 693.97，对照组:8 054.24±975.90， Plt;0.01），致痫后6 h两组大鼠肾组织ERK1/2的表达均达到高峰（致痫后6 h ERK1/2，致痫组:39 217.34±4 443.33，坎地沙坦组：31 924.85±4 383.80，对照组：8 575.24±1 040.82， Plt;0.01），随后逐渐下降，致痫后24 h两组大鼠肾组织ERK1/2表达均回到0 h水平（Pgt;0.05），对致痫组及坎地沙坦干预两组大鼠肾组织ERK1/2蛋白表达进行组间比较结果显示，坎地沙坦组2 h（致痫组：20 229.18±2 067.27，坎地沙坦组：16 878.19±2 693.97，Plt;0.01）、6 h（致痫组：39 217.34±4 443.33，坎地沙坦组：31 924.85±4 383.80，Plt;0.01）、12 h（致痫组：16 610.11±2 953.03，坎地沙坦组：13 393.16±2 269.42， Plt;0.05）ERK1/2表达降低。 结论 ERK1/2在KA致痫大鼠肾组织中表现为短时程表达增加，坎地沙坦可使肾组织ERK1/2表达降低。【Abstract】 Objective To study the effect of candesartan on extracellular signal-regulated kinase (ERK) 1/2 protein expression of renal cells in epilepsy rats induced by kainic acid (KA) and its mechanism. Methods A total of 105 male Wistar rats were randomly divided into three groups: control group (A1-5, n=35), epilepsy group (B1-5, n=35), and candesartan group (C1-5, n=35). The sign 1-5 meant respectively 0, 2, 6, 12, and 24 hours after epilepsy. Epilepsy rat models were made by injecting KA into amygdala under three-dimensional positioning devices. Lavage fixation, paraffin embedding of the renal tissue, and immunohistological test were carried out at different time points after epilepsy was induced, and ERK1/2 protein expression level was tested. Results Compared with the control group, the protein expression of ERK1/2 increased significantly 2 hours after epilepsy in groups B and C (ERK1/2 level 2 hours after epilepsy, group B: 20 229.18±2 067.27, group C: 16 878.19±2 693.97 vs. group A: 8 054.24±975.90, P＜0.01), and both attained its peak 6 hours after epilepsy (ERK1/2 level 6 hours after epilepsy, group B: 39 217.34±4 443.33, group C: 31 924.85±4 383.80 vs. group A: 8 575.24±1 040.82, P＜0.01), and then decreased gradually to the level immediately after epilepsy 24 hours later. There were significant differences in the level of ERK1/2 protein expression between group B and C 2, 6, and 12 hours after epilepsy was induced (2 hours, group B: 20 229.18±2 067.27 vs. group C: 16 878.19±2 693.97, P＜0.01; 6 hours, group B: 39 217.34±4 443.33 vs. group C: 31 924.85±4 383.80, P＜0.01; 12 hours, group B: 16 610.11±2 953.03 vs. group C: 13 393.16±2 269.42, P＜0.05). Conclusions The Extracellular signal-regulated kinase1/2 protein expression of renal tissue in epilepsy rats induced by KA increases shortly after epilepsy. Candesartan can decrease the protein expression of ERK1/2 in the renal tissue of epilepsy rats.
ObjectiveTo evaluate the effects of combined bisoprolol and candesartan therapy on left ventricular hypertrophy and left heart function in in elderly patients with hypertension. MethodsFrom July 2011 to August 2012, 117 elderly inpatients or outpatients with hypertension in our hospital were randomly divided into trial group and control group. Patients in the control group received levamlodipine besylate and bisoprolol, and patients in the trial group received candesartan and bisoprolol. ResultsThere was no statistical difference between the two groups at baseline. Three months later, there was no obvious difference of the blood pressure levels between the two groups (P>0.05). The parameters of left ventricular hypertrophy and left heart function were improved at the end of follow-up in both the two groups, but the parameters of the trial group improved better than the control group (P<0.05). ConclusionIn the elderly patients with hypertension, the combined bisoprolol and candesartan or levamlodipine besylate and bisoprolol therapy can improve left ventricular hypertrophy and left heart function, and the results are better for the combination of bisoprolol and candesartan.