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辛伐他汀对舒张功能不全大鼠心房肌细胞L型钙通道电流及蛋白表达的影响
引用本文:唐惠芳,吴书林,薛玉梅,邓春玉,张文昶.辛伐他汀对舒张功能不全大鼠心房肌细胞L型钙通道电流及蛋白表达的影响[J].中国动脉硬化杂志,2008,16(4):273-277.
作者姓名:唐惠芳  吴书林  薛玉梅  邓春玉  张文昶
作者单位:广东省人民医院心内科,广东省心血管病研究所,广东省广州市,510100
摘    要:目的探讨辛伐他汀对舒张功能不全衰大鼠心房肌细胞L型钙通道电流和L型钙通道相关基因Cav1.2蛋白表达的影响。方法30只雄性SD大鼠,随机分组:对照组、模型组、辛伐他汀组。采用腹主动脉缩窄建立舒张功能不全心力衰竭模型,对照组只开腹和分离腹主动脉。辛伐他汀组大鼠术后灌胃给予辛伐他汀2mg/(kg·d);对照组和模型组大鼠灌胃给予同等量的生理盐水共4周。4周末颈动脉插管记录血流动力学变化,用急性酶解法获得单个大鼠心房肌细胞和标准全细胞膜片钳技术记录通道电流。凝胶电泳法记录心房肌细胞Cav1.2的蛋白表达。结果(1)与对照组比较,模型组大鼠血流动力学显示左心室收缩压和左心室舒张末期压升高,左心室松弛时间常数延长,平均左心室内压最大下降速率下降;辛伐他汀组左心室收缩压、左心室舒张末期压和左心室松弛时间常数明显低于模型组,平均左心室内压最大下降速率明显高于模型组;三组大鼠心率、平均左心室内压最大上升速率以及三组细胞膜电容无明显差异。(2)与对照组比较,模型组L型钙通道电流密度峰值明显少于对照组,激活、失活和复活动力学特征无显著差异;辛伐他汀组L型钙通道电流密度峰值明显大于模型组,失活减慢,激活和复活动力学特征差异均无显著性。(3)与对照组比较,模型组大鼠心房肌细胞Cav1.2蛋白表达水平明显下降;辛伐他汀组心房肌细胞Cav1.2蛋白表达水平明显大于模型组。结论辛伐他汀明显抑制舒张功能不全心力衰竭大鼠心房肌L型钙通道电流下调,此作用与增加心房肌Cav1.2蛋白表达水平有关。

关 键 词:病理学与病理生理学  辛伐他汀  舒张功能不全  心肌细胞  膜片钳  钙通道
收稿时间:2008/1/26 0:00:00
修稿时间:2008/4/14 0:00:00

The Effects of Simvastatin on L-type Calcium Current in Atrial Myocytes of Rats with Diastolic Heart Failure
TANG Hui-Fang,WU Shu-Lin,XUE Yu-Mei,DENG Chun-Yu,and ZHANG Wen-Chang.The Effects of Simvastatin on L-type Calcium Current in Atrial Myocytes of Rats with Diastolic Heart Failure[J].Chinese Journal of Arteriosclerosis,2008,16(4):273-277.
Authors:TANG Hui-Fang  WU Shu-Lin  XUE Yu-Mei  DENG Chun-Yu  and ZHANG Wen-Chang
Affiliation:Department of Cardiology, Guangdong Provincial People''s Hospital, Guangdong Cardiovascular Institute, Guangzhou 510100, China
Abstract:Aim To study the effects of simvastatin on L-type calcium current and Cav1.2 protein levels in atrial myocytes of rats with diastolic heart failure. Methods 30 SD rats were randomly divided into 3 groups: control group, DHF group, Simvastatin group. DHF model was produced by abdominal aortic coarctation in the rats in the operating group. The rats in Simvastatin group were given with Simvastatin 2 mg/(kg·d) by intragastric administration for 4 weeks, the others were treated with equal isotonic Na chloride. After 4 weeks, hemorheology was assessed by catheterization. Single atrial myocytes were isolated by enzymatic dissociation and L-type calcium current were investigated using a whole-cell patch-clamp technique. The expression levels of ICa-L alpha-subunit (Cav1.2) in atrial myocytes were measured by Western-blot analysis. Results (1) Compared with control group, DHF rats exhibited increases in LVSP, LVEDP and Tau. They also showed a decrease in -dp/dtmax. Compared with DHF group, LVSP, LVEDP and Tau were decreased and -dp/dtmax was increased in Simvastatin group. There were no differences in heart rate, the maximum ascendsus ratio for +dp/dtmax and Cm among three groups. (2) Compared with control group, the peak densities of atrial ICa-L in DHF group were decreased, while activation curves, inactivation curves and recovery curves were not altered. Compared with the DHF group, Simvastatin increased the peak density of atrial ICa-L and made the inactivation curves shift to more positive potentials in DHF rats, but did not change activation curves and recovery curves. (3) Campared with control group, DHF rats exhibited decreases in the protein levels of Cav1.2 in atrial myocytes. Simvastatin increased Cav1.2 protein levels in atrial myocytes in DHF rats. Conclusion Simvastatin increases the peak density of atrial ICa-L in DHF rats and the effects are related with the increases in Cav1.2 protein levels.
Keywords:Simvastatin  Diastolic Heart Failure  Myocardial Cell  Patch Clamp  Calcium Current
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