摘要
将刺激合剂注入犬心包腔内使其形成实验性渗出性心包炎,然后分别将尿激酶(UK,4×10000U,治疗组,n=10)和生理盐水(对照组,n=11)注入犬心包腔内.结果,治疗组中UK能显著地降低心包渗出液中纤维蛋白原(Fib)含量(1.91±0.9vs2.6±1.11g/l,P<0.05).病理检查证实,对照组的11只犬全部形成了缩窄性心包炎,治疗组中仅有2只犬发生了心包粘连,两组粘连的发生率有非常显著的差异(20%vs100%、P<0.005).治疗组心包壁层的厚度显著地低于对照组(0.38±0.06vs0.66±0.10mm,P<0.001).用药期间血液中Fib水平(4.51±1.40vs3.85±0.78g/l)、白陶土部分凝血活酶时间(34.81±3.98vs36.40±5.10秒)和凝血酶时间(1.75±1.49vs16.31±1.10秒)均无显著变化(P>0.05).以上结果提示,UK可通过增强心包腔内局部的纤溶活性而防止心包粘连的形成.
After experimental pericarditis with effusion was formed by injecting irritant mixture into canine pericar-dial cavity, urokinase (UK, 4xl0000u, treating group, n = 10 ) and normal saline (control group, n = 11) were in-fused into pericardial cavity of experimental animals re-spectively. As a result,in the treating group UK could sig-nificantly decrease the concentration of fibrinogen (Fib) in the pericardial exudate (1.91±0. 9 vs 2. 6±1. llg/ L,p<0. 05). Pathological examination confirmed that all of 11 dogs in the control group developed constrictive pericarditis (CP) while only two in the treating group. The incidence of pericardial adhesion between two groups showed great significant difference(20% vs 100% ,p< 0. 005). The thickness of parietal pericardium in the treating group was significantly less than that in the con-trol group 0. 38±0. 06 vs 0. 66 ±0. 1 0mm, p < 0. 001). During treatment with UK, the concentration of Fib in the blood, kaoline partial thromboplastin time (KPTT ) and thrombin time ( TT ) didn ' t significantly change (p>0. 05). These results suggested that UK should be effective in preventing the formation of peri-cardial adhesion by increasing locally fibrinolytic activity in the pericardial cavity.
出处
《中国介入心脏病学杂志》
1993年第2期37-40,50,共5页
Chinese Journal of Interventional Cardiology
基金
山东省卫生厅资助课题
关键词
犬缩窄性心包炎
纤维蛋白原
尿激酶
Canine constrictive pericarditis, Fib-rinogen, Urokinase.
