实验性单疱病毒性角膜炎组织形态及超微结构的研究

目的研究单疱病毒性角膜炎（ｈｅｒｐｅｓｓｉｍｐｌｅｘｋｅｒａｔｉｔｉｓ，ＨＳＫ）不同病程阶段角膜组织微观及超微结构的病理变化。方法采用实验性ＨＳＫ原发感染模型，对单疡病毒Ｉ型感染后不同的感染阶段３、７、１４、２１及６０天的兔角膜标本行ＨＥ、Ｍａｌｌｏｒｙ染色于光镜及透射电镜下观察。结果ＨＳＫ时炎性细胞浸润以多形核中性粒细胞为主，急性感染３及７天时角膜基质层内可见炎性细胞与成纤维细胞接触，角膜水肿，严重者内皮层炎性细胞嵌入，电镜下仅２例标本在急性感染阶段中可见单疱·病毒Ｉ型颗粒。结论单疮病毒Ｉ型可直接破坏及损伤机体免疫功能是ＨＳＫ病毒变化的基础，角膜内皮细胞受炎性细胞或免疫细胞浸润可能是基质水肿的一个重要因素。

HIistological and ultrastructural studies of experimental herpetic keratitis in the rabbit

Objective In order to investigate the histological and ultrastructural changes at different post infection days in herpes simplex keratitis(HSK).Methods the corneas of New Zealand white rabbit eyes experimentaly infected with primary HSK were studied by light microscopy and electron microscopy.The histological and ultrastructural changes in the rabbit corneas at 3,7,14,21,60post infection days were investigated by light microscopy with HE,Mallory dyes and electron microscopy.Results Infiltration of corneas with inflammatory cells was foud in rabbit eyes infected with HSK,polymorphonuclear leukocytes being predominant.Contact of inflammatiry cells with fibroblast cells and corneal edema were seen in the stroma on acute post infection days 3 and 7.In severe cases inflammatiry cells incarcerated in the endothelium.Only did two cases of the specimens present with herpes simplex virus type 1 granules in the acute stage under electrorn microscopy.Conclusion the direct HSK-1destruction together with immunopathogenetic injury caused by the boby immune system may serve as the pathologic base of HSK.Decompensation of corneal function due to infilstrtion with inflammatory cells may be responsible for corneal edema.