本文選題：肺血栓栓塞癥 + 重組尿激酶原��； 參考：《軍事醫(yī)學(xué)》2014年12期

【摘要】：目的觀察重組尿激酶原(recombinant prourokinase,r Pro-UK)治療大鼠肺血栓栓塞癥(pulmonary tromboembolus,PTE)后血漿纖溶因子的變化及其意義。方法雄性SD大鼠28只,頸外靜脈注入加熱125-碘(125I)標(biāo)記纖維蛋白原(Fib)自體血栓,復(fù)制大鼠PTE模型,隨機分組如下:1正常對照組;2 PTE 5 d組,即在造模成功后觀察5 d活殺;3 Pro-UK溶栓治療組:分為多次給藥亞組(PTE造模成功后第3天,予Pro-UK 1 mg/kg,后連續(xù)2 d給予Pro-UK 0.25 mg/kg,最后1 d給藥2 h后與PTE 5 d組大鼠同時活殺)和單次給藥亞組(PTE造模成功后第3天給予Pro-UK 1 mg/kg,后連續(xù)2 d給予生理鹽水,活殺時間同PTE 5 d組大鼠)。每組7只,在實驗結(jié)束時經(jīng)頸動脈放血活殺動物,留取血漿標(biāo)本測定尿激酶型纖溶酶原激活物(u-PA)、尿激酶型纖溶酶原激活物受體(u-PAR)、Fib的水平和α2-抗纖溶酶(α2-AP)的活性。結(jié)果 1多次給藥亞組血漿u-PA、u-PAR水平較PTE 5 d組(Pu-PA0.05,Pu-PAR0.01)及單次給藥亞組(Pu-PA0.01,Pu-PAR0.05)明顯升高,與血栓溶解率正相關(guān)(ru-PA=0.766,P0.05;ru-PAR=0.785,P0.05)。2 r Pro-UK溶栓治療后血漿Fib濃度和α2-AP活性與PTE 5 d組比較無顯著差異(P0.05)。結(jié)論 1 r Pro-UK溶栓治療可促進內(nèi)皮細胞合成和分泌u-PA、u-PAR,有助于血栓溶解,這可能是r Pro-UK的一個重要的溶栓機制。2 r Pro-UK多次給藥方案治療大鼠PTE沒有引起繼發(fā)全身纖溶激活,具有纖維蛋白特異性。
[Abstract]:Objective to observe the changes and significance of plasma fibrinolytic factor in rats with pulmonary thromboembolism (PE) treated with recombinant urokinase propranase (Pro-UKR). Methods 28 male SD rats were injected into external jugular vein with 125-iodide 125I) to label fibrinogen (Fib) autothrombus, and the PTE model was established in rats. The rats were randomly divided into two groups as follows: 1 normal control group: 2 PTE 5 d group. The thrombolytic therapy group was divided into two groups: the treatment group was divided into three groups: the third day after the successful establishment of the model, the treatment group was divided into two groups: the third day after the successful establishment of the model, the treatment group was divided into three groups. The rats were given Pro-UK 1 mg / kg for 2 days, Pro-UK 0.25 mg / kg for 2 days, and the rats of PTE 5 d group for 2 h at the same time. The rats in the subgroup were given Pro-UK 1 mg / kg on the 3rd day after the model was successfully established, and then saline was given for 2 days. The killing time was the same as that of PTE group for 5 days. At the end of the experiment, 7 animals in each group were bled and killed through carotid artery. Plasma samples were collected to determine the levels of urokinase-type plasminogen activator (urokinase-type plasminogen activator), urokinase-type plasminogen activator receptor (urokinase type plasminogen activator receptor) and 偽 _ 2-antiplasminase (偽 _ 2-AP). Results (1) the plasma u-PA-PA-PA-PAR level in the multiple administration subgroup was significantly higher than that in the PTE 5-day group (Pu-PA0.05Pu-PAR0.01) and the single-dose subgroup (Pu-PA0.01Pu-PAR0.05). There was no significant difference in plasma Fib concentration and 偽 2-AP activity between the two groups after thrombolytic therapy, and there was no significant difference in plasma Fib concentration and 偽 2-AP activity between the two groups after thrombolytic therapy. Conclusion 1r Pro-UK thrombolytic therapy can promote endothelial cell synthesis and secretion of u-PA-PAu-PAR. this may be an important thrombolytic mechanism of r Pro-UK. 2 r Pro-UK regimen does not induce secondary systemic fibrinolytic activation in rats. It has the specificity of fibrin.
【作者單位】： 首都醫(yī)科大學(xué)附屬北京朝陽醫(yī)院 呼吸與危重癥醫(yī)學(xué)科;北京呼吸疾病研究所;國家衛(wèi)生和計劃生育委員會(原衛(wèi)生部)中日友好醫(yī)院;鄭州大學(xué)第一附屬醫(yī)院;
【分類號】：R563.5
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本文編號：1931613