An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization.
An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization.
复制标题
评估白细胞在实验诱导的角膜血管化发病机制中的作用。
DOI：
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发表时间：
1975
影响因子：
6
通讯作者：
G. Klintworth
中科院分区：
文献类型：
--
作者：
C. Fromer;G. Klintworth
在仓鼠颊囊室中进行的角膜移植研究表明，只有当组织首先被白细胞浸润时，血管才会侵入角膜。鉴于这一观察结果，在各种实验模型中对角膜血管化之前和伴随的事件进行了比较研究。使用各种已建立的方法来诱导角膜血管化，包括将角膜暴露于有害试剂，将抗原角膜内注射到致敏动物中，以及维持动物缺乏维生素A或核黄素的饮食。在所有研究的模型中，角膜血管化是炎症反应的修复阶段的表现。在所有模型中，角膜的明显白细胞浸润先于并伴随角膜血管化。虽然在不同的模型中的病变在几个方面有所不同，所有的模型显示三个阶段的血管化：早期血管前阶段的白细胞浸润，第二阶段，血管持续在角膜中的白细胞的情况下。血管形成前的潜伏期与初始白细胞浸润的时间直接相关。白细胞浸润延迟的模型显示随后的血管长入延迟。相反，在有快速和广泛的白细胞浸润的实验中，也有早期和增强的角膜血管增生反应。在所研究的各种模型中，白细胞浸润和随后血管长入角膜的部位相互重叠。这些数据进一步支持白细胞是角膜血管化的先决条件以及白细胞产生一种或多种刺激定向血管生长的因子的假设。
Studies of corneal explants in the hamster cheek pouch chamber have demonstrated that blood vessels invade the cornea only if the tissue is first infiltrated by leukocytes. In view of this observation, a comparative study of the events that precede and accompany corneal vascularization was undertaken in various experimental models. A variety of established methods were used to induce corneal vascularization, including exposure of the cornea to noxious agents, intracorneal injection of antigens into sensitized animals, as well as maintaining animals on diets deficient in vitamin A or riboflavin. In all models studied, the corneal vascularization was a manifestation of the reparative phase of the inflammatory response. A conspicuous leukocytic infiltrate of the cornea preceded and accompanied the corneal vascularization in all of the models. Although the lesions varied in several respects in the different models, all models displayed three phases with regard to vascularization: an early prevascular phase of leukocytic infiltration, a second phase where blood vessels persisted in the cornea in the absence of leukocytes. The latent period that preceded vascularization was directly related to the time of the initial leukocytic infiltration. The models in which a delay occurred in the leukocytic invasion displayed a subsequent delay in the vascular ingrowth. Conversely, in experiments where there was a rapid and extensive leukocytic invasion, there was also an early and enhanced corneal vasoproliferative response. In the various modesl investigated, the sites of the leukocytic infiltration and subsequent vascular ingrowth into the cornea paralleled each other. The data further support the hypotheses that leukocytes are a prerequisite to corneal vascularization and that leukocytes produce one or more factors which stimulate directional vascular growth.