Tengroth B, Ammitzbøll T
Acta Ophthalmol (Copenh). 1984 Dec;62(6):999-1008. doi: 10.1111/j.1755-3768.1984.tb08452.x.
The pressure theory is still predominant in explaining the pathophysiology of the chronic open angle glaucoma. An insufficient drainage system resulting in an increased intraocular pressure is the basis for this theory. The pressure will exert an effect upon the optic disc which either directly on the nerve fibres or indirectly via the vascular system will result in a characteristic optic atrophy. The collagen fibres, both in the trabecular meshwork of the anterior chamber and in the lamina cribrosa of the optic disc, form a mesh through which the aqueous humour and the nerve fibres, respectively, pass through the wall of the eye. A hypothesis explaining the pathophysiology of this disease, and based on the assumption that there is a primary change in the collagen molecules, resulting in a weaker structure than normal both in the trabeculae and in the laminae, is forwarded. The structures analysed for the content of hydroxyproline, hydroxylysine and proline were the trabecular meshwork, the sclera and the lamina cribrosa. Three categories of autopsy eyes were studied, i.e. normal eyes, glaucomatous eyes, and eyes under a suspicion of glaucoma. In the normal eyes, the collagen composition in the trabecular meshwork was different from that in the sclera and the lamina cribrosa. There is also a difference in the composition between the sclera and the lamina cribrosa. In glaucoma, the content and/or the composition of the collagen molecules in the lamina were significantly changed. In the eyes under suspicion of glaucoma the same changes as in the glaucomatous eyes could be demonstrated. However, 5 of the 7 eyes in this category had no demonstrable nerve atrophy. The findings suggest that the change in collagen pattern is primary. This study has not demonstrated which types of collagen are present or the physical properties of this collagen. Further tests to demonstrate the different types of collagen and their rigidity are planned.
压力理论在解释慢性开角型青光眼的病理生理学方面仍然占据主导地位。该理论的基础是引流系统不足导致眼内压升高。这种压力会对视盘产生影响，要么直接作用于神经纤维，要么通过血管系统间接作用，从而导致特征性的视神经萎缩。前房小梁网和视盘筛板中的胶原纤维形成一个网，房水和神经纤维分别通过这个网穿过眼球壁。基于胶原分子存在原发性变化，导致小梁和筛板结构比正常结构更脆弱这一假设，提出了一种解释该疾病病理生理学的假说。分析羟脯氨酸、羟赖氨酸和脯氨酸含量的结构是小梁网、巩膜和筛板。研究了三类尸检眼睛，即正常眼睛、青光眼眼睛和疑似青光眼的眼睛。在正常眼睛中，小梁网中的胶原组成与巩膜和筛板中的不同。巩膜和筛板之间的组成也存在差异。在青光眼中，筛板中胶原分子的含量和/或组成发生了显著变化。在疑似青光眼的眼睛中，可以证明与青光眼眼睛有相同的变化。然而，这一类别的7只眼睛中有5只没有可证实的神经萎缩。这些发现表明胶原模式的变化是原发性的。这项研究尚未证明存在哪些类型的胶原或这种胶原的物理特性。计划进行进一步的测试以证明不同类型的胶原及其硬度。
