血小板和纤维蛋白在愈合过程中的作用：血管生成和胶原蛋白合成的体内研究。

UNLABELLED

The signals that initiate repair are poorly characterized. These studies investigate the capacity of platelets and fibrin to initiate angiogenesis, fibroplasia, collagen synthesis and monocyte migration in the rabbit cornea assay.

METHODS

Autologous platelets and platelet-free fibrin were isolated from rabbit blood. Released and control platelet preparations and autologous and commercial fibrin were implanted in rabbit corneas.

RESULTS

Thrombin-released platelets produced angiogenesis and opacification. Histology showed fibroplasia, corneal thickening, and neovascularization. Collagen synthesis was elevated to twice control levels in thrombin-activated platelet preparations. Various control platelet preparations produced no angiogenesis, no opacification, and no histologic change. All fibrin injections elicited a cellular exudate from the limbal vessels, followed by angiogenesis and corneal opacification. Histology showed a mononuclear infiltrate with neovascularization and fibroplasia. Control injections of rabbit skin collagen and fibroblasts produced no response.

未标记

启动修复的信号特征尚不明确。这些研究在兔角膜试验中探究了血小板和纤维蛋白启动血管生成、纤维组织形成、胶原合成及单核细胞迁移的能力。

方法

从兔血中分离出自体血小板和无血小板纤维蛋白。将释放型和对照型血小板制剂以及自体和商用纤维蛋白植入兔角膜。

结果

凝血酶释放的血小板产生血管生成和浑浊。组织学显示有纤维组织形成、角膜增厚和新生血管形成。在凝血酶激活的血小板制剂中，胶原合成升高至对照水平的两倍。各种对照血小板制剂未产生血管生成、浑浊及组织学变化。所有纤维蛋白注射均引起来自角膜缘血管的细胞渗出，随后出现血管生成和角膜浑浊。组织学显示有单核细胞浸润伴新生血管形成和纤维组织形成。注射兔皮肤胶原和成纤维细胞的对照未产生反应。