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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。
Objective To observe the changes of endothelial and fibrinolytic function in atrial fibrillation induced by rapid atrial pacing and the effects of cilazapril in dogs with atrial fibrillation. To explore the mechanism of prethrombotic state of atrial fibrillation and its prevention and treatment. Methods From January 2004 to August 2004, 16 Mongolian dogs were randomly divided into control group (n = 8), cilazapril group (n = 8) Atrial pacing in atrial (AOO) mode 400 / min for 6 weeks, the establishment of atrial fibrillation dog model. Cinerapril (1 mg / kg) was administered daily from 1 week before pacing in cilostazol group until the end of pacing. Before ventricular pacing, venous blood was collected 6 weeks after pacing, plasma vWF was measured vWF, Ang II, t-PA and PAI-1. Results After atrial pacing for 6 weeks, Ang Ⅱ level in control group was significantly higher than that before pacing ([(349.9 ± 28.3) ng / L vs 198.4 ± 19.4 ng / L, P <0 · 01]. There was no significant increase of AngⅡ in cilazapril group (P> 0.05). The vWF in plasma increased after fast pacing [(109.7 ± 19.8)% vs (33 · 9 ± 5 · 9)%, P <0.01). The plasma vWF after cilazapril pacing was also increased, but significantly lower than that of the control group (P <0.01) The PAI-1 antigen levels were significantly higher in patients with PAI-1 than those with PAI-1 (t = PA: (12.7 ± 2.1) ng / L vs. (8.9 ± 1.5) ng / L, P <0.01] (24.4 ± 3.9) ng / L vs (15.4 ± 2.4) ng / L, P <0.01). Both of the two groups also increased after pacing High level is lower than the control group. Conclusion Chronic atrial pacing leads to activation of canine renin-angiotensin system (RAS), dysfunction of endothelial function and fibrinolysis. Cilazapril can block the activation of RAS and improve endothelial and fibrinolysis to varying degrees. Angiotensin-converting enzyme inhibitors (ACEIs) may be used in the prevention and treatment of atrial fibrillation.