CAJ | 학술논문

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＜0.05)，同时血浆PRA、AngⅡ水平及PAI-1活性增高(P＜0.05)；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。
목적：검측심력쇠갈(HF)－심기허대서순배신소혈관긴장소계통(RAS)급섬용매원격활물억제제(PAI-1)활성변화，토론HF－심기허시기허혈어여RAS격활대내원성섬용계통적관계급기의의。방법：건립대서동정맥루(AVF)HF－심기허화대조조모형(가수술조)，검측좌심실공능，용방면법화발색저물법검측혈장신소활성(PRA)、혈관긴장소라마수(AngⅡ)농도급PAI-1변화，병진행량조간비교。결과：여가수술조화술전비교，HF－심기허조대서술후출현좌심공능불전，좌실수축압강저、서장말압증고(P＜0.05)，동시혈장PRA、AngⅡ수평급PAI-1활성증고(P＜0.05)；수착심공능개선，혈장PRA、AngⅡ수평급PAI-1활성하강。결론：HF－심기허시RAS격활대도치궤체섬용계통공능실형유중요작용，가용이해석엄중심공능불전환자혈액정고응상태，병차발생혈전전새질병위험증고적원인，가능위심기허치기허혈어적병리생리기출。
Objective: To explore the relationship between cardiac Qideficiency 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.