介入放射学杂志
介入放射學雜誌
개입방사학잡지
Journal of Interventional Radiology
2015年
10期
890-896
,共7页
动脉瘤%动物模型%颈动脉%血流动力学%组织病理学
動脈瘤%動物模型%頸動脈%血流動力學%組織病理學
동맥류%동물모형%경동맥%혈류동역학%조직병이학
aneurysm%animal model%carotid artery%hemodynamics%histopathology
目的:建立犬动物模型,研究特定血流动力学变化及动脉壁退化是否会导致动脉瘤发生发展。方法建立18只犬颈总动脉(CCA)新分叉模型,随机分组为弹力蛋白酶处理组(EBG,n=9)和分叉模型对照组(CBG,n=9);同时设弹力蛋白酶处理直段CCA对照组(ESG,n=3)。术后即刻,术后12周、24周分别行血管造影及血流动力学分析,术后12周和24周行组织病理学分析。结果血管造影显示EBG组5只犬模型CCA分叉顶部出现新生动脉瘤形成,瘤体平均直径(3.2±0.4) mm,CBG组和ESG组均未观察到新生动脉瘤形成;EBG组新生动脉瘤在随访期间未见破裂。组织学分析显示EBG组内层弹力膜不连续、弹力纤维断裂、肌层变薄、平滑肌细胞减少,炎性细胞(巨噬细胞)浸润及MMP-2、MMP-9表达增多(与CBG组和ESG组对比,P<0.001)。血流动力学分析显示EBG组分叉顶部壁面切应力减低、血流速度减慢、相对压力和总压力最高,动脉壁重塑后均恢复正常。结论本实验表明动脉壁退化和动脉分叉处血流动力学作用可导致犬模型新生动脉瘤形成。
目的:建立犬動物模型,研究特定血流動力學變化及動脈壁退化是否會導緻動脈瘤髮生髮展。方法建立18隻犬頸總動脈(CCA)新分扠模型,隨機分組為彈力蛋白酶處理組(EBG,n=9)和分扠模型對照組(CBG,n=9);同時設彈力蛋白酶處理直段CCA對照組(ESG,n=3)。術後即刻,術後12週、24週分彆行血管造影及血流動力學分析,術後12週和24週行組織病理學分析。結果血管造影顯示EBG組5隻犬模型CCA分扠頂部齣現新生動脈瘤形成,瘤體平均直徑(3.2±0.4) mm,CBG組和ESG組均未觀察到新生動脈瘤形成;EBG組新生動脈瘤在隨訪期間未見破裂。組織學分析顯示EBG組內層彈力膜不連續、彈力纖維斷裂、肌層變薄、平滑肌細胞減少,炎性細胞(巨噬細胞)浸潤及MMP-2、MMP-9錶達增多(與CBG組和ESG組對比,P<0.001)。血流動力學分析顯示EBG組分扠頂部壁麵切應力減低、血流速度減慢、相對壓力和總壓力最高,動脈壁重塑後均恢複正常。結論本實驗錶明動脈壁退化和動脈分扠處血流動力學作用可導緻犬模型新生動脈瘤形成。
목적:건립견동물모형,연구특정혈류동역학변화급동맥벽퇴화시부회도치동맥류발생발전。방법건립18지견경총동맥(CCA)신분차모형,수궤분조위탄력단백매처리조(EBG,n=9)화분차모형대조조(CBG,n=9);동시설탄력단백매처리직단CCA대조조(ESG,n=3)。술후즉각,술후12주、24주분별행혈관조영급혈류동역학분석,술후12주화24주행조직병이학분석。결과혈관조영현시EBG조5지견모형CCA분차정부출현신생동맥류형성,류체평균직경(3.2±0.4) mm,CBG조화ESG조균미관찰도신생동맥류형성;EBG조신생동맥류재수방기간미견파렬。조직학분석현시EBG조내층탄력막불련속、탄력섬유단렬、기층변박、평활기세포감소,염성세포(거서세포)침윤급MMP-2、MMP-9표체증다(여CBG조화ESG조대비,P<0.001)。혈류동역학분석현시EBG조분차정부벽면절응력감저、혈류속도감만、상대압력화총압력최고,동맥벽중소후균회복정상。결론본실험표명동맥벽퇴화화동맥분차처혈류동역학작용가도치견모형신생동맥류형성。
Objective To establish carotid artery bifurcation aneurysm in canine, and to clarify whether specific hemodynamic insult in combination with arterial wall degeneration will lead to the occurrence and development of aneurysms. Methods New bifurcation aneurysm model of common carotid artery (CCA) was successfully established in 18 dogs, which were randomly divided into the elastase-treated bifurcation group (EBG,n=9) and the control bifurcation group (CBG,n=9). Three dogs were treated with elastase insult to both straight sections of CCA and were used as elastase-treated straight section group (ESG,n=3). Angiographic and hemodynamic analysis was conducted immediately after the operation, as well as 12 and 24 weeks after the operation. Histopathological examination was performed 12 and 24 weeks after the operation. Results Angiography showed that new aneurysm (mean diameter 3.2 ±0.4 mm) was formed at the apex of CCA bifurcation in 5 dog models of EBG group, while no new aneurysm was observed in both CBG and ESG groups. In EBG group, no rupture of the new aneurysm occurred during the follow-up period. Histological analysis revealed that in EBG group the inner elastic lamina was discontinued, the elastic fiber was disrupted, the muscle layer became thinned, the smooth muscle cells were reduced, and the inflammatory cell (macrophage) infiltration as well as the expressions of MMP-2 and MMP-9 were increased;these changes were statistically significant when compared with those in CBG group and ESG group (P<0.001). Postoperative hemodynamic analysis indicated that in EBG group the wall shear stress at the apex of CCA bifurcation was reduced, the blood flow velocity was decreased, with the relative and total pressure being the highest;all the above changes returned to normal after arterial wall remodeling. Conclusion The results of this study indicate that the arterial wall degeneration and the hemodynamic effect at the apex of CCA bifurcation can lead to new aneurysm formation in canine model.