CALCIUM TRANSIENTS IN SINGLE MYOCYTES AND MEMBRANOUS ULTRASTRUCTURES DURING THE DEVELOPMENT OF CARDIAC-HYPERTROPHY AND HEART-FAILURE IN RATS

被引:17
作者
KURAMOCHI, T
HONDA, M
TANAKA, K
ENOMOTO, K
HASHIMOTO, M
MORIOKA, S
机构
[1] SHIMANE MED UNIV,DEPT INTERNAL MED 4,IZUMO,SHIMANE 693,JAPAN
[2] SHIMANE MED UNIV,DEPT PHYSIOL 2,IZUMO,SHIMANE 693,JAPAN
[3] SHIMANE MED UNIV,DEPT PHYSIOL 1,IZUMO,SHIMANE 693,JAPAN
关键词
CALCIUM TRANSIENTS; CARDIAC HYPERTROPHY; CARDIAC MYOCYTES; HEART FAILURE; MEMBRANOUS ULTRASTRUCTURE; MONOCROTALINE;
D O I
10.1111/j.1440-1681.1994.tb02664.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 RVB progressed. Single myocytes were separated from the RV during different stages of RVH. Fura-2/AM-loaded cells were held 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.
引用
收藏
页码:1009 / 1018
页数:10
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