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

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.

Keywords: Absorbable; Arterial stenosis; Embolization; Gelatin sponge.

Fig. 1

Microscopic images of segmental arteries within 1 week after embolization with GSPs. A. Four days after embolization. There is partially organized thrombus (arrow), and aggregation of macrophages and polymorphonuclear leukocytes between GSPs (dotted arrow). Three layers of vessel wall are preserved. B. One week after embolization. There is focal intimal destruction with transmural inflammation (arrow). Medial and adventitial layers are slightly thickened with proliferation of smooth muscle cells (dotted arrow). Internal elastic lamina is intact (hematoxylin and eosin staining, original magnification × 20). GSPs = gelatin sponge particles

Fig. 2

Microscopic images of interlobar arteries 2 weeks after embolization with GSPs. A. There is partial resorption of GSPs. Note focal dehiscence of internal elastic lamina with propagation of transmural inflammation (arrows). There are some giant cells, indicating foreign body reaction (dotted arrow) (hematoxylin and eosin staining, original magnification × 20). B. There is destruction of all 3 layers in some arteries, resulting from extravasation of GSPs (arrows) (hematoxylin and eosin staining, original magnification × 10). GSPs = gelatin sponge particles

Fig. 3

Microscopic images of interlobar arteries 3 weeks after embolization with GSPs. A. Embolized GSPs have completely disappeared, resulting in recanalization. Original lumen is mainly filled with thick organized thrombi (arrow). B. Immunohistochemical staining for smooth muscle actin, showing proliferation of smooth muscle cells in media and thickened intima with migration of smooth muscle cells from media, and interruption of internal elastic lamina (dotted arrow). Migrating smooth muscle cells are mainly distributed around recanalized arterial lumen (arrows). C. Completion angiography, showing diffuse luminal narrowing and multifocal stenosis (arrows) in recanalized arteries of lower pole, compared with non-embolized arteries of upper pole. GSPs = gelatin sponge particles

Fig. 4

Microscopic image of interlobar artery 4 weeks after embolization with gelatin sponge particles. There are no inflammatory cells. Completely organized thrombus attached to vessel wall, and decreased proliferation of smooth muscle cells in media is observed. Internal elastic lamina has multifocal loss of continuity (arrows) (immunohistochemical staining for smooth muscle actin, original magnification × 20).