青光眼已成为当今世界第一大不可逆的致盲眼病。已有的研究证实，青光眼的原发部位是巩膜筛板。高眼压导致筛板变形，挤压视神经乳头造成不可逆的视觉损失，这一青光眼发病机制已得到了广泛认可。在青光眼发病过程中，筛板的厚度被确定并不发生变化，但由于高眼压引起的高强度荷载作用，筛板结缔组织变形直至发生塑性变形、筛孔拉伸、筛板上变形不均并在局部出现应力集中现象。但由于筛板尺寸较小、结构复杂，在临床和实验研究中难度较大，因此为更加深入理解筛板变形与青光眼发病机理的定量关系，需要合理的力学模型来研究筛板的受力与变形。与Kirchhoff经典薄板理论相比，Reissner板理论对直法线假设进行了修正，充分考虑了板的横向剪切变形。因此，以Reissner板理论为基础建立的筛板模型，弹性刚度既不过大，也不至于过于柔软，更能合理反映筛板变形的真实情形。本文以Reissner板理论建立的筛板力学模型为基础，研究了筛板上筛孔附近的应力集中问题，横向剪切变形的机制以及筛板的变形对视神经乳头血液循环的影响，从而帮助理解和解释青光眼视神经损伤机制。得到以下结论：

1. 在筛板的变形过程中，由于筛孔的存在，造成了局部应力急剧增加的应力集中现象。在筛孔孔口周围应力集中效应最大，应力增大了2.87倍。筛板边缘附近筛孔孔口应力达到最大值，约为眼内压的3倍。
2. 在高应力的作用下，筛孔变形程度也随之增大。由于筛板在高眼压荷载下，应力分布的不均匀性，使得筛板不同位置上的筛孔变形程度也大不相同。筛板边缘附近的筛孔变形最为明显，由于应力集中，此处应变增大至塑性变形阶段，损伤不可恢复。
3. 眼内压升高，会直接降低视神经乳头供血的睫状后动脉内扩散压强。同时，眼内压升高还会使筛板变形压迫穿过其中的睫状后动脉血管，一方面使血管内产生明显的相对负压，进一步降低扩散压强，导致血管内血流减少，并在动脉间形成分水区，干扰血液循环，造成视神经乳头供血不足。另一方面，筛板变形挤压血管，使血流在血管内壁上产生高剪应力和高剪应力梯度，损伤动脉，破环视神经乳头的血液循环。

Glaucoma is the first cause of irreversible blindness in the world. It has been widely accepted that elevated intraocular pressure (IOP) can disrupt the structure of the lamina cribrosa (LC) and damage the optic nerve head (ONH) at the level of the LC, which leads to irreparable visual loss. Some facts have been found in the glaucoma progression. Elevated IOP causes the LC deflect without affecting its thickness. The deformation of the tissue is plastic. Lamina pores are elongated. Stresses in the LC are not uniform and concentrated in some region. Due to the small size and complexed structure, researching on the LC is quite difficult both clinically and experimentally. Thus, a proper biomechanical model is urgently needed to deeper the understanding of force acting and deformation of the LC. Compared to Kirchhoff’s thin plate theory, Reissner’s plate theory remotes the assumption, that the normal line of the middle plane of the plate before the deformation still remains the normal line of the middle plane after the deformation, and takes shear deformation of the plate into consider. Reissner’s plate theory is more suitable for modeling the LC. In this thesis, we discuss stress concentration caused by lamina pores, shear deformation of the sheets and their effects on the circulation of ONH, based on the model of the LC. The main conclusions are summarized as followed:

1. Lamina pores cause stress concentration in the LC, it can only affect the local region near the pore and reduce rapidly in a further distance.
2. As stresses become several times greater because of the concentration, strains in the local region also increase. Since the distribution of stresses in the LC is inhomogeneous, the deformation of lamina pores varies in different LC regions. The greatest deformation occurs at the rim of the LC, and becomes plastic and unrecoverable due to stress concentration. This may contribute to the fact that the glaucomatous visual loss often begins on the edge of the eyesight.
3. Elevated IOP can not only reduce perfusion pressure directly, but also force the LC to squeeze arterioles that supply the ONH blood. Blood flow in these arterioles induces a lower blood pressure, which will also reduce the perfusion pressure. Then, the blood flow becomes smaller, and watershed zones appear between the arterioles. They both cause the ischemia of the ONH. The squeezed arterioles also cause the blood flow make greater shear stress and shear stress grad on the wall. This may damage the arterioles, and interrupt the circulation of the ONH.