筛板血管系统的三维重建及青光眼视神经损害的机理研究

Glaucoma, a leading cause of irreversible blindness, is effecting 60 million patients in the world. Unfortunately, the pathogenesis of glaucomatous optic neuropathy (GON) is still unclear. The debate between the mechanical and the vascular theory lasted past 150 years and still is, which lead to the standstill in the treatment and prevention of glaucoma. Our groundwork: In theory, we analyzed the anatomical relationship between the selective injury of nerve fibers and damage of lamina cribrosa, deduced the regularity of damage to lamina cribrosa based on the regularity of the visual field defect and found out the vascular pathogenesis of GON. Finally, we proposed a hypothesis: The abnormality of Zinn-Haller arterial rings lead to the early GON. This hypothesis, for the first time in the world, adequately explained the great variations in susceptibility to damage and the patterns of damage seen in this syndrome. In practice, we mastered the three-dimensional reconstruction based on the serial pathological sections and microvascular castings and were able to acquire the serial pathological sections of lamina cribrosa of a normal human eye. This project is about investigating the relationship between abnormality of Zinn-Haller arterial rings and the early GON based on the 3-D reconstruction and microvascular castings of glaucomatous human eye. Our hypothesis is an original one, the verification of which will fill gaps in the vascular theory on GON, ending the dispute between the mechanical and the vascular theory, and direct the clinical treatment in a new direction.

青光眼作为首位的不可逆性致盲性眼病，危及了全球6000万人口的视力。但是关于青光眼视神经损害的确切机理，目前仍不清楚，150年来，机械学说和血管学说争论不休，致使青光眼的治疗与预防手段停滞不前。我们的前期工作：理论上，剖析了视神经纤维束缺损与筛板病变之间的解剖关系，并由视野缺损的规律推及了筛板病变的规律，从而揭示了青光眼选择性视神经损害的血管机制, 提出了：筛板动脉环异常假说。该假说首次合理的解释了青光眼视野缺损的多样性和视神经损害易感度的多样性。实践上，掌握了连续病理切片三维成像技术和微血管铸型技术，初步完成了正常人眼筛板的连续病理切片。本课题拟行: 青光眼人眼及猴眼筛板连续病理切片的三维重建和微血管铸型技术，证实：筛板动脉环异常与青光眼早期视神经纤维损害的相关性。本假说为原创，假说的证明将填补青光眼视神经损害血管学说的机制空白，结束两种学说对峙的局面，并为青光眼的临床治疗指引新的方向。

青光眼作为首位的不可逆性致盲性眼病，其视神经损害的确切机理，一直是国内外研究的热点。机械学说和血管学说争论不休，本课题针对血管学说提出了：筛板动脉环异常假说。具体内容如下：筛板动脉环的吻合支可能存在狭窄区段，相应的筛板动脉就是“问题动脉”；眼压在筛板周边部，主要是弹性纤维环处，造成了巨大的剪切力，弹性纤维环反复发生形变，诱发或加重了从中穿行的‘问题动脉'发生病变，导致相应的筛板区域缺血。 . 本课题旨在证实筛板Zinn-Haller动脉环异常与早期青光眼视神经缺损的关系。通过建立青光眼动物模型证实：筛板动脉缺血可导致对应部位的视神经纤维的进行性损伤。通过对青光眼患者筛板血流密度与视神经、视野损伤相关性进行分析，证实：筛板血流密度减少出现在视神经纤维变薄、视野缺损之前，视野损伤多样性是由于筛板动脉环缺血的多样性决定的，即筛板动脉环某区域血供减少，造成筛板相应区域缺血，导致视神经纤维变薄、视野缺损。从而论证了我们的筛板动脉环异常假说。. 本课题合理的解释了青光眼视野缺损的多样性和视神经损害易感度的多样性，证实：筛板动脉环异常与青光眼早期视神经纤维损害的相关性。填补青光眼视神经损害血管学说的机制空白，并为青光眼的临床治疗指引新的方向。