| 吴齐雁,胡小萍,李德新,李贺,贺威琼,江浪进.心气虚证大鼠循环肾素血管紧张素系统激活与血浆纤溶酶原激活物抑制剂活性变化的实验研究[J].,2001,(5):367-369 |
| 心气虚证大鼠循环肾素血管紧张素系统激活与血浆纤溶酶原激活物抑制剂活性变化的实验研究 |
| Qi Deficiency and Blood Stasis and Circulatory Renin-Angiotensin System as well as Plasminogen Activator Inhibitor Activity in Rats with Cardiac Qi Deficiency Syndrome |
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| DOI： |
| 中文关键词: 心气虚证 气虚血瘀 肾素血管紧张素系统 血浆纤溶酶原激活物抑制剂 心力衰竭模型 |
| 英文关键词:Heart Qi deficiency Syndrome Qi deficiency and blood stasis renin angiotensin system plasminogen activator inhibitor activity heart failure model |
| 基金项目:国家自然科学基金部分资助! (No .39470 838) |
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| 中文摘要: |
| 目的 :检测心力衰竭 (HF) -心气虚大鼠循环肾素血管紧张素系统 (RAS)及纤溶酶原激活物抑制剂 (PAI 1)活性变化 ,讨论HF -心气虚时气虚血瘀与RAS激活对内源性纤溶系统的关系及其意义。方法 :建立大鼠动静脉瘘 (AVF)HF -心气虚和对照组模型 (假手术组 ) ,检测左心室功能 ,用放免法和发色底物法检测血浆肾素活性 (PRA)、血管紧张素罗马数 (AngⅡ )浓度及PAI 1变化 ,并进行两组间比较。结果 :与假手术组和术前比较 ,HF -心气虚组大鼠术后出现左心功能不全 ,左室收缩压降低、舒张末压增高 (P <0 0 5) ,同时血浆PRA、AngⅡ水平及PAI 1活性增高 (P <0 0 5) ;随着心功能改善 ,血浆PRA、AngⅡ水平及PAI 1活性下降。结论 :HF -心气虚时RAS激活对导致机体纤溶系统功能失衡有重要作用 ,可用以解释严重心功能不全患者血液呈高凝状态 ,并且发生血栓栓塞疾病危险增高的原因 ,可能为心气虚致气虚血瘀的病理生理基础 |
| 英文摘要: |
| Objective: To explore the relationship between cardiac Qi deficiency Syndrome and effect of circulatory renin angiotensin system (RAS) and endogenous fibrinolytic system in rats with heart failure (HF). Methods: Plasma RAS levels and plasminogen activator inhibitor (PAI 1) activity were measured in 2 groups of rats: the sham operated group (Group A) and the HF with Heart Qi deficiency Syndrome model group (Group B) established by making arteriovenous fistula. Using radioimmunoassay and chromatography, plasma renin activity (PRA) and angiotensin Ⅱ (Ang Ⅱ) levels and PAI 1 activity were determined before, immediately after and 30 days after the surgical operation respectively. Results: After the operation was completed in Group B the left ventricular dysfunction revealed, left ventricular systolic pressure decreased and end diastolic pressure increased (P<0 05), PRA and Ang Ⅱ level and PAI 1 activity increased significantly, as compared with those in Group A and before modeling (P<0 05). With cardiac function improved, the plasma PRA, Ang Ⅱ level and PAI 1 activity lowered in Group B comparing with those immediately after modeling (P<0 05). Conclusion: The activation of RAS is associated with the endogenous fibrinolyticim balance, and play an important role in endogenous fibrinolytic system dysfunction in HF with Heart Qi deficiency Syndrome and Qi deficiency blood stasis, which was helpful to explain that cause of hypercoagulant state in HF patients and increase the risk of suffering from embolism thrombotic diseases, and might be the pathogenetic basis of Heart Qi deficiency induced Qi deficiency blood stasis. |
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