Tuba A, Kálmán M
Department of Anatomy, Histology, and Embryology, Semmelweis University of Medicine, Budapest, Hungary.
J Neural Transplant Plast. 1997 Mar-Jun;6(2):97-103. doi: 10.1155/NP.1997.97.
The present study focused on the early events of vascularization of intraocular cerebral transplants. Telencephalic pieces of rat embryos (E15) were transplanted into the anterior eye chamber of adult rats in deep ketamine-xylazine narcosis. At 3-, 4-, 5-, 6-, or 7-day postoperative survival periods, the rats were perfused and the transplants, with their iridic beds, were processed into serial, semi-thin sections. In 3- and 4-day transplants, neither dilated (perfused) nor collapsed blood vessels were found, but tissue defects, without proper wall and filled by non-nucleated (mature, host) erythrocytes, were seen. On post-operative day 5, large sinusoids were seen lines by endothelium and free of blood cells (as a consequence of perfusion). On days 6 and 7, the usual, although large, blood vessels were found. Our results suggest that the critical period of transplant vascularization is between postoperative days 4 and 5, and that the original vessels of donor tissue degenerate and disappear during the first postoperative days and thus, do not participate directly in transplant vascularization. Our hypothesis is that vascular invasion begins with the opening of host blood vessels into clefts formed by degeneration of graft tissue. For a period, a hemostasis occurs in these blood-filled lacunae, and then endothelium invasion from host vessels forms the proper wall. The transplant vasculature develops from these large sinusoids. The results challenge the role of the pre-existing donor vessels in transplant vascularization. A possible explanation of such paradoxical results is that the donor tissue must reach a stage of maturation to receive the ingrowing vessels, either host vessels, and the presence of vessels in the donor brain is the sign of this stage of maturation but has no direct role in transplant vascularization.
本研究聚焦于眼内脑移植血管化的早期事件。将大鼠胚胎(E15)的端脑片段在氯胺酮-赛拉嗪深度麻醉下移植到成年大鼠的前房。在术后3、4、5、6或7天的存活期,对大鼠进行灌注,将移植体及其虹膜床制成连续的半薄切片。在术后3天和4天的移植体中,未发现扩张(灌注)或塌陷的血管,但可见组织缺损,没有合适的管壁,且由无核(成熟的、宿主的)红细胞填充。术后第5天,可见由内皮细胞衬里且无血细胞(由于灌注)的大血窦。在第6天和第7天,发现了通常的、尽管较大的血管。我们的结果表明,移植血管化的关键时期在术后第4天和第5天之间,并且供体组织的原始血管在术后最初几天退化并消失,因此不直接参与移植血管化。我们的假设是,血管侵入始于宿主血管向由移植组织退化形成的裂隙开放。在一段时间内,这些充满血液的腔隙会发生止血,然后宿主血管的内皮细胞侵入形成合适的管壁。移植血管系统从这些大血窦发育而来。这些结果对移植血管化中预先存在的供体血管的作用提出了挑战。对这种矛盾结果的一种可能解释是,供体组织必须达到成熟阶段才能接受长入的血管,无论是宿主血管,并且供体脑中血管的存在是这个成熟阶段的标志,但在移植血管化中没有直接作用。