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环孢素治疗后通过血管同种异体移植实现轴突再生。

Axon regeneration through blood vessel allografts after cyclosporine treatment.

作者信息

Gulati A K

机构信息

Department of Anatomy, Medical College of Georgia, Augusta.

出版信息

J Neurosurg. 1989 Jan;70(1):115-20. doi: 10.3171/jns.1989.70.1.0115.

DOI:10.3171/jns.1989.70.1.0115
PMID:2909670
Abstract

The present study describes the usefulness of blood vessel allografts to repair gaps in rat peripheral nerve after immunosuppression with cyclosporine. Isogeneic strains of rats with known histoincompatibility were used for this study. A 10-mm gap was created in the peroneal nerve of host Fischer rats. The gap was bridged by a 12-mm section of internal carotid artery removed from a Buffalo strain of rat. The host rats were divided into two groups. One group received no immunosuppression, whereas the other group was treated with cyclosporine. Untreated control rats immunologically rejected the allografted vessels and were unable to support host axonal regeneration through them. On the other hand, in cyclosporine-treated rats the allografted vessels survived. The regenerating host axons reorganized to form a functional nerve within the vessel conduit. The regenerated axons persisted even after rejection of the allografted vessel caused by cessation of immunotherapy. These results show that blood vessel allografts can serve as an effective conduit for reorganization of regenerated nerves and can bridge gaps in peripheral nerves.

摘要

本研究描述了在使用环孢素进行免疫抑制后,血管异体移植对修复大鼠周围神经缺损的有效性。本研究使用了具有已知组织相容性的同基因大鼠品系。在宿主Fischer大鼠的腓总神经上制造一个10毫米的缺损。该缺损由从水牛大鼠品系中取出的一段12毫米的颈内动脉桥接。宿主大鼠被分为两组。一组不接受免疫抑制,而另一组用环孢素治疗。未经治疗的对照大鼠在免疫上排斥异体移植的血管,并且无法支持宿主轴突通过它们再生。另一方面,在接受环孢素治疗的大鼠中,异体移植的血管存活了下来。再生的宿主轴突重新组织,在血管管道内形成一条功能性神经。即使在因停止免疫治疗导致异体移植血管被排斥后,再生的轴突仍然存在。这些结果表明,血管异体移植可以作为再生神经重组的有效管道,并能桥接周围神经的缺损。

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Axon regeneration through blood vessel allografts after cyclosporine treatment.环孢素治疗后通过血管同种异体移植实现轴突再生。
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引用本文的文献

1
Arterial bridging for repair of peripheral nerve gap: a comparative study.
Acta Neurochir (Wien). 1993;121(3-4):181-6. doi: 10.1007/BF01809272.