摘要
为探讨压力负荷性肥大心肌中肿瘤坏死因子α和血管紧张素Ⅱ的表达及其与心肌肥大的关系 ,采用腹主动脉缩窄法复制压力超负荷心肌肥大动物模型 ,于术后 4 2天测定心肌肥大指数 ,并用放射免疫法测定血浆及左心室肌血管紧张素Ⅱ含量 ;用酶联免疫吸附法测定血清及左心室肌肿瘤坏死因子α含量。结果发现 ,术后 4 2天左心室心肌明显肥大 ;心室肌肿瘤坏死因子α、血管紧张素Ⅱ含量分别比假手术组增高约 6倍和 1倍 (P <0 .0 1) ;主动脉缩窄术后开搏通干预能显著抑制心肌肥大的发展 ,使心室肌肿瘤坏死因子α含量下降 6 4 .14 % (P <0 .0 1) ,但未恢复到假手术组水平 (P <0 .0 1) ;心室肌血管紧张素Ⅱ含量下降 4 5 .73% (P <0 .0 1) ,与假手术组无显著性差异。结果提示 ,压力负荷增加心肌血管紧张素Ⅱ含量 ,引起心肌组织肿瘤坏死因子α含量升高 ,可能是压力超负荷心肌肥大的主要调控路径之一。
Aim To clarify the relation of expression change of tumor necrosis factor-α (TNF-α) and angiotensin Ⅱ (AngⅡ)in hypertrophic mayocardial on stress load. Methods Sampling blood and extirpate heart after 42 days in the cardiac hypertrophy model of exceed stress load were made by abdomen aorta-constriction; determining hypertrophic exponent and the concentration of AngⅡin the plasma and myocardium by Ratio-immunity; determining TNF-α in serum and left ventricle by enzyme-linked immunoadsordent assay. Results Left ventricle showed obvious hypertrophy after operation 42 days; the concentration of TNF-α and AngⅡ in myocardium heighten 6 folds and 1 fold than controls (P<0.01); Being treated by Captopril can restrain the progress of left ventricle hypertrophy after operation and descend the content of TNF-α in myocardium 64.14% (P<0.01), but can not descend to the level of sham-operated group (P<0.01). Being the content of AngⅡ descend 45.73% (P<0.01)and had no marked significance to the level of sham-operated group. Conclusions The activation of cardiac renin-angiotensin system (RAS) by excess stress load result to heighten TNF-α in myocardium and it is probably one of the major adjusting path of myocardial hypertrophy.
出处
《中国动脉硬化杂志》
CAS
CSCD
2003年第6期517-519,共3页
Chinese Journal of Arteriosclerosis
基金
陕西省卫生厅青年科研基金 ( 2 0 0 0 0 9)项目
