【摘要】 目的观察心房快速起搏诱发心房颤动犬内皮和纤溶功能的变化及西拉普利对其影响,探讨房颤血栓前状态的机制及防治对策。方法2004年1月至8月于哈尔滨医科大学第一临床医学院动物实验中心选杂种犬16只,随机分为对照组(n=8)、西拉普利组(n=8),在右心房以单心房(AOO)模式400/min起搏6周,建立房颤犬模型。西拉普利组起搏前1周开始每天服用西拉普利(1mg/kg),直至起搏结束,分别于起搏前、起搏6周后采静脉血,测血浆血管性血友病因子(vWF)、血管紧张素Ⅱ(AngⅡ)、组织型纤溶酶原激活剂(t-PA)、纤溶酶原激活剂抑制物-1(PAI-1)。结果心房快速起搏6周,对照组犬血浆AngⅡ较起搏前明显增高,[(349·9±28·3)ng/L对(198·4±19·4)ng/L,P<0·01];西拉普利组AngⅡ无明显升高(P>0·05);快速起搏后血浆vWF升高[(109·7%±19·8)%对(33·9±5·9)%,P<0·01),西拉普利起搏后血浆vWF亦升高,但却明显低于对照组(P<0·01)];起搏6周后血浆t-PA、PAI-1抗原均明显升高[t-PA:(12·7±2·1)ng/L对(8·9±1·5)ng/L,P<0·01][PAI-1:(24·4±3·9)ng/L对(15·4±2·4)ng/L,P<0·01];西拉普利组起搏后两者亦升高但两者升高程度低于对照组。结论慢性心房快速起搏导致犬肾素-血管紧张素系统(RAS)激活、内皮功能及纤溶功能失调,西拉普利可以阻断RAS激活,不同程度改善内皮和纤溶功能。血管紧张素转换酶抑制剂(ACEI)可能用于房颤血栓防治。更多还原

【Abstract】 Objective To observe endothelial and fibrinolytic functions of atrial fibrillation(AF)dogs induced by chronic rapid atrial pacing and effects of cilazapril on it and to investigate the mechanism of thrombogenesis in AF.Methods From January to August of 2004,16 dogs were randomly divided into control group(n=8)and cilazapril group(n=8).All dogs were paced at 400 bpm for 6 weeks by AOO pacemaker.The dogs in cilazapril group received cilazapril(1mg·kg-1·d-1)from 1week before pacing to 6 weeks after pacing.Plasma angiotensinⅡ(AngⅡ),von Willebrand factor(vWF),tissue-type plasminogen activator(t-PA)and plasminogen activator inhibitors-1(PAI-1)level were measured before and after rapid pacing respectively.Results After rapid atrial pacing,plasma AngⅡ,vWF,t-PA and PAI-1 level increased significantly in control group dogs(AngⅡ:(349.9±28.3)ng/L vs(198.4±19.4)ng/L,P<0.01;vWF:(109.7±19.8)%vs(33.9±5.9)%,P<0.01;t-PA:(12.7±2.1)ng/L vs(8.9±1.5)ng/L,P<0.01;PAI-1:(24.4±3.9)ng/L vs(15.4±2.4)ng/L,P<0.01;before vs after pacing,respectively).Compared with control group,the plasma vWF,t-PA and PAI-1 level decreased to some extent in cilazapril group.Conclusion Activated RAS results in endothelial and fibrinolytic dysfunctions which may play an important role in chronic rapid atrial pacing dogs.Cilazapril could inhibit RAS and improve endothelial and fibrinolytic dysfunctions in AF.更多还原