中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2009年
5期
509-513
,共5页
组织因子途径抑制物%基因转染%颈动脉损伤%血栓形成%显微镜检查%电子%扫描
組織因子途徑抑製物%基因轉染%頸動脈損傷%血栓形成%顯微鏡檢查%電子%掃描
조직인자도경억제물%기인전염%경동맥손상%혈전형성%현미경검사%전자%소묘
Tissue factor pathway inhibitor%Gene therapy%Carotid artery injuries%Thrombosis formation%Microscopy%electron%scanning
目的 观察人组织因子途径抑制物(tissue factor pathway inhibitor,TFPI)基因在兔颁动脉损伤血栓形成的作用.方法 大耳白兔40只,体质量2.5～3.0 kg.将白兔按体质量随机分为4组:腺病毒介导的TFPI基因(Ad-TFPI)转染组、腺病毒介导的LacZ基因(Ad-LzcZ)转染组、磷酸盐缓冲液(PBS)组和对照组,每组10只.对照组不进行任何处理,另3组用PTCA球囊导管对白兔右侧颈动脉进行损伤,损伤处分别用DisDatch转基因导管按组别局部注射转染Ad-TFPI、Ad-LacZ液和PBS各0.2 ml.转染10 d后,采用相同方法对白兔颈动脉损伤处进行二次损伤,对照组进行第1次损伤,损伤后立即恢复血流.30 min后处死白兔,分别取出损伤侧和对侧颈总动脉,沿长轴剪开、展平,2%戊二醛固定,扫描电镜下观察4组白兔损伤处动脉管壁血小板聚集及纤维素(血栓)形成情况.结果 扫描电镜下,正常未经任何损伤的颈动脉管腔内可见血管内皮细胞结构完整,排列整齐;对照组在球囊损伤后血管内皮不完整,有部分血小板聚集,血管肇上无纤维素生成;Ad-TFPI组在二次损伤后血小板聚集增加,但血管壁上未见纤维素形成;Ad-LacZ组和PBS组可见皿管壁上有大量的纤维素形成和红细胞堆积.血管壁血栓形成阳性率组间比较差异有统计学意义(χ2=14.95,P<0.01);其中Ad-TFPI组(20%)低于Ad-LacZ组(80%,χ2=7.20,P<0.01)和PBS组(70%,χ2=5.05,P<0.05),高于对照组(10%,χ2=0.39,P>0.05);Ad-LacZ组(80%)高于对照组(10%,χ2=9.90,P<0.01),也高于PBS组(70%,χ2=0.27,P>0.05);PBS组(70%,)高于对照组(10%,χ2=7.50,P<0.01).结论 二次球囊损伤法可造成大量血栓形成;腺病毒表达载体TFPI可以抑制动脉损伤后纤维素沉积.
目的 觀察人組織因子途徑抑製物(tissue factor pathway inhibitor,TFPI)基因在兔頒動脈損傷血栓形成的作用.方法 大耳白兔40隻,體質量2.5～3.0 kg.將白兔按體質量隨機分為4組:腺病毒介導的TFPI基因(Ad-TFPI)轉染組、腺病毒介導的LacZ基因(Ad-LzcZ)轉染組、燐痠鹽緩遲液(PBS)組和對照組,每組10隻.對照組不進行任何處理,另3組用PTCA毬囊導管對白兔右側頸動脈進行損傷,損傷處分彆用DisDatch轉基因導管按組彆跼部註射轉染Ad-TFPI、Ad-LacZ液和PBS各0.2 ml.轉染10 d後,採用相同方法對白兔頸動脈損傷處進行二次損傷,對照組進行第1次損傷,損傷後立即恢複血流.30 min後處死白兔,分彆取齣損傷側和對側頸總動脈,沿長軸剪開、展平,2%戊二醛固定,掃描電鏡下觀察4組白兔損傷處動脈管壁血小闆聚集及纖維素(血栓)形成情況.結果 掃描電鏡下,正常未經任何損傷的頸動脈管腔內可見血管內皮細胞結構完整,排列整齊;對照組在毬囊損傷後血管內皮不完整,有部分血小闆聚集,血管肇上無纖維素生成;Ad-TFPI組在二次損傷後血小闆聚集增加,但血管壁上未見纖維素形成;Ad-LacZ組和PBS組可見皿管壁上有大量的纖維素形成和紅細胞堆積.血管壁血栓形成暘性率組間比較差異有統計學意義(χ2=14.95,P<0.01);其中Ad-TFPI組(20%)低于Ad-LacZ組(80%,χ2=7.20,P<0.01)和PBS組(70%,χ2=5.05,P<0.05),高于對照組(10%,χ2=0.39,P>0.05);Ad-LacZ組(80%)高于對照組(10%,χ2=9.90,P<0.01),也高于PBS組(70%,χ2=0.27,P>0.05);PBS組(70%,)高于對照組(10%,χ2=7.50,P<0.01).結論 二次毬囊損傷法可造成大量血栓形成;腺病毒錶達載體TFPI可以抑製動脈損傷後纖維素沉積.
목적 관찰인조직인자도경억제물(tissue factor pathway inhibitor,TFPI)기인재토반동맥손상혈전형성적작용.방법 대이백토40지,체질량2.5～3.0 kg.장백토안체질량수궤분위4조:선병독개도적TFPI기인(Ad-TFPI)전염조、선병독개도적LacZ기인(Ad-LzcZ)전염조、린산염완충액(PBS)조화대조조,매조10지.대조조불진행임하처리,령3조용PTCA구낭도관대백토우측경동맥진행손상,손상처분별용DisDatch전기인도관안조별국부주사전염Ad-TFPI、Ad-LacZ액화PBS각0.2 ml.전염10 d후,채용상동방법대백토경동맥손상처진행이차손상,대조조진행제1차손상,손상후립즉회복혈류.30 min후처사백토,분별취출손상측화대측경총동맥,연장축전개、전평,2%무이철고정,소묘전경하관찰4조백토손상처동맥관벽혈소판취집급섬유소(혈전)형성정황.결과 소묘전경하,정상미경임하손상적경동맥관강내가견혈관내피세포결구완정,배렬정제;대조조재구낭손상후혈관내피불완정,유부분혈소판취집,혈관조상무섬유소생성;Ad-TFPI조재이차손상후혈소판취집증가,단혈관벽상미견섬유소형성;Ad-LacZ조화PBS조가견명관벽상유대량적섬유소형성화홍세포퇴적.혈관벽혈전형성양성솔조간비교차이유통계학의의(χ2=14.95,P<0.01);기중Ad-TFPI조(20%)저우Ad-LacZ조(80%,χ2=7.20,P<0.01)화PBS조(70%,χ2=5.05,P<0.05),고우대조조(10%,χ2=0.39,P>0.05);Ad-LacZ조(80%)고우대조조(10%,χ2=9.90,P<0.01),야고우PBS조(70%,χ2=0.27,P>0.05);PBS조(70%,)고우대조조(10%,χ2=7.50,P<0.01).결론 이차구낭손상법가조성대량혈전형성;선병독표체재체TFPI가이억제동맥손상후섬유소침적.
Objective To observe the effects of tissue factor pathway inhibitor(TFPI) on thrombosis formation in rabbit carotid arteries after ballon injury. Methods Fouty rabbits with the weight 2.5-3.0 kg were respectively divided into 4 groups, Ad-TFPI, Ad-LacZ, PBS and normal control groups. The normal control group was not given any treatment and other 3 groups were given 0.2 ml Ad-TFPI, Ad-LacZ or PBS reproduced by the Dispatch catheter respectively after the PTCA balloon iniury on the right carotid arteries. Ten days after gene transfer the repeated balloon injury was performed in the 3 groups, and the first balloon injury was performed in the normal control group by the same method. The carotid blood flow was recovered immediately after the injury. Thirty minutes later all the animals were sacrificed. The injured carotid arteries and one part of contralateral normal artery were cut down, scissored along the long axis, flattened and fixed in the 2% glutaral. The platelet aggregation and thrombosis formation on the luminal surfaces was observed under electron microscope. Results The electron microscope results showed that the vascular endothelial cell structure was integrated and lined up in order in the nomal artery which had no any injury. After the balloon injury in the normal control group, the structure of the endothelial cell was disintegrated, and there was some platelet aggregation but no fibrosis formation. A large amount of platelet aggregated but no fibrosis formed in Ad-TFPI group after the repeated balloon injury. A large amount of fibrosis formed and red cells piled up in the Ad-LacZ and PBS group. The positive rate of thrombosis formation among groups had siginificant differences(χ2=14.95, P<0.01). The positive rate in Ad-TFPI group(20%) was lower than that in Ad-LacZ group(80%, χ2=7.20, P<0.01) and PBS group(70%, χ2=5.05, P<0.05), but was higher than that in the normal control group(10%, χ2=0.39, P>0.05). The positive rate in Ad-LacZ group(80%) was higher than in the normal control group(10%, χ2=9.90, P<0.01) and in the PBS group(70%, χ2=0.27, P> 0.05). The positive rate in PBS group(70%) was higher than that in the normal control group(10%, χ2=7.50, P< 0.01). Conclusions The repeated balloon injury method can cause a large amount of fibrosis formation in the rabbit carotid. TFPI gene inhibits thrombosis formation in balloon-injured rabbit carotid arteries.
