MORPHOLOGICAL ALTERATIONS AND THEIR FUNCTIONAL INTERPRETATION IN THE HYPERTROPHIED MYOCARDIUM OF GOLDBLATT HYPERTENSIVE RATS

被引:34
作者
WENDTGALLITELLI, MF
EBRECHT, G
JACOB, R
机构
[1] Institute of Physiology II, University of Tuebingen
关键词
Compensatory stage; Connective tissue; Experimental cardiac hypertrophy; Isometric tension; Mitochondria; Myofibrils; Shortening velocity; Stereology;
D O I
10.1016/0022-2828(79)90441-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Goldblatt rats with a mean blood pressure of 190 mmHg show a left ventricular hypertrophy (4 and 8 weeks after operation) of 40 to 50% in comparison to controls. Sarcomere length is not increased significantly. Stereological measurements on myocardial cell components show that contractile mass is significantly increased between 4 and 8 weeks after operation in hypertrophied hearts, partially at the expense of mitochondria. The volume occupied by mitochondria decreases, while mitochondrial structure remains normal during the early stage. The T- and sarcotubular systems also increase. Golgi complex is enlarged and consists of dilated cisternae. Disarrangements of myofibrils are observed. The 24-week group of hypertrophied hearts shows high heterogeneity: in some animals vessel wall alterations and diffuse fibrosis are observed. The hearts of the remaining operated rats show quantitative morphological changes characteristic of the compensatory stage without evidence of degenerative alterations. Physiological alterations indicate that maximum isometric tension development increases in the early compensatory stage of hypertrophy; this fact can be partially explained by the increased mass of contractile structures. The greatest functional impairment with regard to isometric tension development and Vmax is observed in those 24-week animals showing evident histological alterations outside the muscle cell. The increase in the sarcotubular system and the persistence of decreased Vmax under high Ca2+ concentration suggests that not all changes in mechanical parameters can be attributed to alterations in excitation-contraction coupling. © 1979.
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页码:275 / +
页数:1
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