大鼠压力性左室肥大及其逆转的超微结构改变

Ultrastructural changes of left ventricular hypertrophy and regression induced by pressure-overload in rats

目的：为探讨压力性左室肥厚心肌细胞的逆转情况。方法：采用 Ｇｏｌｄｂｌａｔ 大鼠肾血管性高血压动物模型，造成压力性左室肥大。用切除缩窄肾的方法使发生高血压的动物血压降至正常，左室的压力负荷减轻，肥大的左室发生逆转（ｒｅｇｒｅｓｓｉｏｎ） 。用体视学方法定量分析心肌细胞内肌原纤维与线粒体所占体积在肥大与逆转过程的相对变化，探讨心肌细胞内能量产生与消耗这两个相关因素的关系。结果：严重肥大的心肌细胞经过与过度负荷等时段的降压去负荷治疗，可使心脏重量减轻，心肌细胞直径缩小，在形态学上部分恢复正常，但其超微结构及线粒体，肌原纤维体方面的改变仍未恢复，严重的高血压并有严重的间质纤维化病变的则为不可逆病变。结论：降压可使部分压力性左室肥大心肌细胞在形态学上恢复正常，但伴有严重恶性高血压及心脏间质纤维化病变者难以恢复正常。

Aim:To evaluate the ultrastructure and morphometric changes of hypertrophied and regreessive myocardium. Methods:The expreriment adopted Goldblatt hypertensive animal model which induced by clipping left kidney artery. Results: After removal of left kiddney, the blood pressure reduced to normal, hypertrophied myocardium regressed. Conclusion: The results showed that after pressure reduced to normal, heart weight and myocardial diameter reduced to normal nearly but mitochondrial ( M t), myofibrile ( M f) volumetric percentage and M t/ M f ratio didn't regress to normal.