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大鼠心肌肥大和心力衰竭发展过程中单个心肌细胞内的钙瞬变及膜超微结构

Calcium transients in single myocytes and membranous ultrastructures during the development of cardiac hypertrophy and heart failure in rats.

作者信息

Kuramochi T, Honda M, Tanaka K, Enomoto K, Hashimoto M, Morioka S

机构信息

Fourth Department of Internal Medicine, Shimane Medical University, Japan.

出版信息

Clin Exp Pharmacol Physiol. 1994 Dec;21(12):1009-18. doi: 10.1111/j.1440-1681.1994.tb02664.x.

DOI:10.1111/j.1440-1681.1994.tb02664.x
PMID:7736651
Abstract
  1. We examined changes in intracellular calcium transients of separated single myocytes from the right ventricle (RV) of the rat heart during the change from adaptation to maladaptation in response to a pressure overload. 2. Right ventricular hypertrophy (RVH) secondary to pulmonary hypertension was induced by a subcutaneous injection of monocrotaline. Developed tensions of the RV-free wall were decreased as RVH progressed. Single myocytes were separated from the RV during different stages of RVH. Fura-2/AM-loaded cells were field stimulated, and changes in calcium transients were measured by Olympus OSP-3 system. We also examined membranous ultrastructures (sarcoplasmic reticulum, mitochondria, surface caveolae) involved in calcium metabolism in the hearts using scanning electron microscopy. 3. We observed characteristic changes in calcium transients during the change from adaptation to maladaptation, and also found that one parameter (amplitude) of calcium transients appeared to be correlated with the changes in the number of sarcoplasmic reticulum. 4. These results provided some insights into the mechanism of calcium handling of hypertrophied heart in response to a pressure overload from adaptation to maladaptation especially when stimulatory frequency was high, and suggested that heart rate control is a very important factor for the treatment of patients with congestive heart failure.
摘要
  1. 我们研究了大鼠心脏右心室(RV)分离的单个心肌细胞在从适应压力超负荷到适应不良转变过程中细胞内钙瞬变的变化。2. 通过皮下注射野百合碱诱导继发于肺动脉高压的右心室肥厚(RVH)。随着RVH进展,右心室游离壁的舒张张力降低。在RVH的不同阶段从右心室分离单个心肌细胞。用Fura-2/AM负载细胞进行场刺激,并通过奥林巴斯OSP-3系统测量钙瞬变的变化。我们还使用扫描电子显微镜检查了心脏中参与钙代谢的膜超微结构(肌浆网、线粒体、表面小窝)。3. 我们观察到从适应到适应不良转变过程中钙瞬变的特征性变化,还发现钙瞬变的一个参数(幅度)似乎与肌浆网数量的变化相关。4. 这些结果为肥厚心脏在从适应到适应不良的压力超负荷反应中钙处理机制提供了一些见解,特别是当刺激频率较高时,并表明心率控制是治疗充血性心力衰竭患者的一个非常重要的因素。

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