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Experimental over-stretching of the femoral artery in the sheep in situ

, : Experimental over-stretching of the femoral artery in the sheep in situ. Der Unfallchirurg 93(1): 15-18

Arterial lesions associated with fractures or luxations are thought to be caused by an overstretching mechanism. In this paper we would like to elucidate this mechanism in an animal model. Eight sheep (mean age 1.7 years, mean weight 67 kg) were placed under general anesthesia and their femoral arteries prepared. Before stretching, a lesion was induced by crushing the artery with a blunt household wire clipper, so that the adventitial layer was not damaged. With a balloon catheter (inserted through a vessel branch) rupture of the intimal and medial layers was induced. The adventitia was lengthened in situ by tearing with the fingers until a sand-glass form occurred. Two to three minutes later the arteries were occluded proximally and distally so that traction could be stopped. After removal, the vessels were fixated immediately in formaldehyde and embedded in methylacrylate. Using the van Gieson elastica technique, 4- to 6-microns sections were stained. On histological examination of the proximal stump, a thrombus was located in the lumen surrounded by adventitial tissue, which was sheared off from the medial layer for some distance. There was no invagination of the medial layer. The histology of the distal arterial stump is shown in Fig. 6. The findings are similar to those in Fig. 5; in particular, the behavior of the adventitia can be seen here, the thrombus is enveloped by adventitial fibers. These findings can be explained by the three-dimensional network of the adventitia. With regard to the large amount of fibers, a direct platelet-collagen-interaction may be responsible for this thrombus.


PMID: 2315708

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