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实验性明胶海绵栓塞兔肾模型后动脉损伤的评估。

Evaluation of arterial impairment after experimental gelatin sponge embolization in a rabbit renal model.

机构信息

Department of Radiology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.

Department of Hospital Pathology, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.

出版信息

Korean J Radiol. 2015 Jan-Feb;16(1):133-8. doi: 10.3348/kjr.2015.16.1.133. Epub 2015 Jan 9.

DOI:10.3348/kjr.2015.16.1.133
PMID:25598681
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4296261/
Abstract

OBJECTIVE

Arterial stenosis is a major obstacle for subsequent interventional procedures. We hypothesized that the stenosis is caused by gelatin sponge embolization and performed an experimental study in a rabbit renal model.

MATERIALS AND METHODS

A total of 24 rabbits were embolized with porcine gelatin sponge particles injected into the renal arteries. Four rabbits were sacrificed on 1 day, 4 days, 1 week, 2 weeks, 3 weeks, and 4 weeks after embolization. Microscopic evaluations were performed on hematoxylin-eosin and smooth muscle actin immunohistochemical stained sections.

RESULTS

Gelatin sponge particles were mainly observed in the segmental and interlobar arteries. Transmural inflammation of the embolized arterial wall and mild thickening of the media were observed 1 week after embolization. Resorption of the gelatin sponge and organization of thrombus accompanied by foreign body reactions, were observed from 2 to 4 weeks after embolization. Microscopic images of the 3 weeks group showed vessel lumens filled mostly with organized thrombi, resulting in severe stenosis. Additionally, vessels showed a thickened intima that contained migrating smooth muscle cells and accompanying interruption of the internal elastic lamina. The migrating smooth muscle cells were distributed around the recanalized arterial lumen.

CONCLUSION

Gelatin sponge embolization may induce arterial stenosis by causing organized thrombus and intimal hyperplasia, which consists of migrating smooth muscle cells and intimal collagen deposits.

摘要

目的

动脉狭窄是后续介入治疗的主要障碍。我们假设狭窄是由明胶海绵栓塞引起的,并在兔肾模型中进行了一项实验研究。

材料和方法

将猪明胶海绵颗粒注入肾动脉,对 24 只兔子进行栓塞。栓塞后 1 天、4 天、1 周、2 周、3 周和 4 周,有 4 只兔子被处死。对苏木精-伊红和平滑肌肌动蛋白免疫组化染色切片进行了显微镜评估。

结果

明胶海绵颗粒主要观察到在节段性和小叶间动脉中。栓塞动脉壁的壁内炎症和中膜轻度增厚在栓塞后 1 周观察到。从栓塞后 2 周到 4 周,观察到明胶海绵的吸收和血栓的形成以及伴随的异物反应。3 周组的显微镜图像显示血管腔主要充满了已形成的血栓,导致严重狭窄。此外,血管内膜增厚,包含迁移的平滑肌细胞和伴随的内弹性膜中断。迁移的平滑肌细胞分布在再通的动脉腔周围。

结论

明胶海绵栓塞可能通过引起血栓形成和内膜增生导致动脉狭窄,内膜增生由迁移的平滑肌细胞和内膜胶原沉积组成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/1f9d3bb1d9a0/kjr-16-133-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/7e2197e224a6/kjr-16-133-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/0e815c50bc0f/kjr-16-133-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/2fe50ac52ce9/kjr-16-133-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/1f9d3bb1d9a0/kjr-16-133-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/7e2197e224a6/kjr-16-133-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/0e815c50bc0f/kjr-16-133-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/2fe50ac52ce9/kjr-16-133-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c168/4296261/1f9d3bb1d9a0/kjr-16-133-g004.jpg

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