摘要
以淋巴细胞为研究模型，用随机对照和电镜细胞化学方法，对４２例扩张型心肌病患者在常规抗心力衰竭治疗基础上加用卡托普利、能气朗（Ｃ＿ｏＱ＿（１０））或安慰剂，经平均２．５个月观察，随着心功能改善，血浆血管紧张素Ⅱ水平恢复，于加用卡托普利及能气朗者，外周淋巴细胞线粒体增生程度减轻；线粒体膜磷脂损伤性改变得到修复（Ｐ均＜０．０１）。而在常规抗心力衰竭治疗基础上加用安慰剂者则改变不明显。提示卡托普利及Ｃ＿ｏＱ＿（１０）对心衰患者线粒体膜磷脂损伤有修复作用。
Abstract The membrane-phospholipid(MPL)injury of myocardial cells may play an important role in the development of heart failure. In the present study,peripheral lymphocytes were used as a study model from which the protective and reparative effects of captopril and coenzyme Q10 (CoQ10) on mitochondrial (Mit) membrane-phospholipid injury were observed. Fourty-two hospitalized patients with dilated cardiomyopathy ( DCM), on conventional antiheart-failure therapy,were divided into three groups at tandom and Capoten/Neuquinone 10 / placebo were added respectively.The menbrane phospholipid localization was proceeded by modified Dermer's tricomplex flocculation. After a mean of 75.5 days observation, in captopril and CoQ10 groups, with the improvement of heart function and the decreased circulating AII (angiotensin II) level turned back, the proliferation degree of Mit of the lymphocytes decreased and the Mit membrane-phospholipid injury got repaired in certain degree, the percentages of the lymphocytes with less than 5 Mit per a lymphocyte increased (60.0±9.4 vs 72.0 ± 6.8% for captopril, 55.0 ±8.9% vs 73.1± 9.8 % for CoQ10 . P < 0.001); the percentages of Mit with intact membrane-phospholipid localization increased (59.1± 8.1 vs 72.0 ±9.4% for captopril;. 56.6±9.3 vs 73.8 ± 9.4% for CoQ10. P<0.001). But no difference was found in either the proliferation or the membrane-phospholipid injury in the controls.In conclusion, captopril and CoQ10 have a beneficial role in the protection and the reparation of the Mit injury in DCM.
出处
《中华心血管病杂志》
CSCD
北大核心
1994年第1期49-51,共3页
Chinese Journal of Cardiology
基金
卫生部科研基金
