Decreased myocyte tension development and calcium responsiveness in rat right ventricular pressure overload
Decreased myocyte tension development and calcium responsiveness in rat right ventricular pressure overload
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DOI：
10.1161/01.cir.95.9.2312
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发表时间：
1997-05-06
期刊：
影响因子：
37.8
通讯作者：
deTombe, PP
中科院分区：
文献类型：
--
作者：
Fan, DS;Wannenburg, T;deTombe, PP
研究背景：终末期心肌肥厚的收缩功能障碍是以心肌细胞功能异常为基础的。然而，收缩功能降低是否与收缩蛋白功能的改变有关目前尚不清楚。方法和结果从右室肥厚(RVH)大鼠和对照组大鼠分离的单层皮肤心肌细胞测定了收缩力量、张力和钙反应性。肺动脉缩窄36周可诱发RVH，并伴有明显的心肌细胞肥大。肌细胞连接到从力传感器和马达延伸出来的微管上。等长力是在肌节长度(SLS)处的大范围钙浓度下测量的。RVH组最大用力增加：SL=2.0µm时1.20+/-0.10 mg比1.62+/-0.13 mg；SL=2.3µm时1.33+/-0.10 mg比1.84+/-0.15 mg(P
Background The contractile dysfunction observed in endstage myocardial hypertrophy has at its base an abnormality in myocyte function. However, whether depressed contractile function is related to an alteration in contractile protein function is presently unknown.Methods and Results Contractile force, tension, and calcium responsiveness were measured in single-skinned myocytes isolated from rats with right ventricular hypertrophy (RVH) and control rats. RVH was induced by pulmonary artery constriction for 36 weeks and was associated with significant myocyte hypertrophy. Myocytes were attached to micropipettes that extended from a force transducer and motor. Isometric force was measured over a wide range of calcium concentrations at mio sarcomere lengths (SLs). Maximal force was increased in the RVH group: 1.20+/-0.10 versus 1.62+/-0.13 mg at SL=2.0 mu m and 1.33+/-0.10 versus 1.84+/-0.15 mg at SL=2.3 mu m (P