Genesis of light-induced avian glaucoma.
Genesis of light-induced avian glaucoma.
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光诱发禽青光眼的起源。
DOI：
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发表时间：
1974
期刊：
影响因子：
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通讯作者：
T. Boyd
中科院分区：
文献类型：
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作者：
A. Kinnear;J. Lauber;T. Boyd
光致鸟型青光眼的特点是眼大、眼压高、流出能力低、房水体积减少。在这项研究中，我们已经确定了几个发生在早期病理过程中的病变，从5天到28天。7日龄时，角膜乳酸脱氢酶(LDH)活性较低，水液LDH活性较高。到28天时，房水LDH是正常水平的3.5倍，角膜！乳酸脱氢酶降低了10%。9天后房水体积缩小，3周后眼球明显增大。眼压和C在此期间保持正常，尽管C后来受损(在6周时)，并且在大约16周时眼压的动态平衡控制被破坏。虽然角膜和玻璃体体积改变的主要原因(S)尚未确定，但它们出现的时间差异表明这两种损伤可能是相互独立的。角膜LDH的改变提示内皮通透性的早期改变，允许过多的酶丢失到房水。在连续光照(24L/0D)下饲养的家鸡会出现严重的眼部形态和生理损伤，最终导致青光眼和失明。我们将这种情况称为光致鸟类青光眼。尽管人类开角型青光眼是一个严重的临床问题，但很少有实验动物会患上这种疾病，据我们所知，在其他任何动物中，这种情况都不能根据研究人员的意愿而加剧。光诱导性鸟型青光眼与眼球重量和直径增加、中心曲率减少、流出功能受损和眼内压升高有关。1‘-眼球增大和屈光不正在流出功能受损前几周就可被检测到，眼压在疾病过程中甚至更晚才会升高。8虽然虹膜角膜角狭窄，但在24L/0D下饲养的雏鸡虹膜切除术未能改变发展中的青光眼的进程，如果瞳孔阻塞导致虹膜爆炸，则可能是预期的。1当24L/0D的鸟类被不透明的视觉遮盖器遮盖时，眼睛的放大程度并不比没有遮盖的眼睛小，这表明这是一种全身性的而不是局部的病因。然而，这些积极的发现几乎没有提供关于光诱导的鸟类青光眼的病因的线索。我们技术的改进现在已经使监测孵化后7天的雏鸡的房水流体动力学成为可能：我们在这里详细说明这些青光眼前的早期变化。我们还测量了…
Light-induced avian glaucoma is characterized by eye enlargement, high intraocular pressure (IOP), low outflow facility (C), and reduced aqueous space volume. In this study we have identified several lesions occurring in the early pathologic process, from five to 28 days of age. At seven days, comeal lactic dehydrogenase (LDH) is low and aqueous LDH is high. By 28 days, aqueous LDH is 3.5 times normal levels and cornea! LDH is reduced by 10 per cent. By nine days, aqueous space volume is reduced, and eye enlargement is evident by three weeks. IOP and C remain normal during this period, although C is later impaired (at six weeks) and homeostatic control of IOP breaks down at approximately 16 weeks. Though the primary cause(s) for the dimensional changes in cornea and vitreous body have not been identified, the difference in the time of their appearance indicates that these two lesions may be independent of one another. The comeal LDH change suggests early alteration in endo-thelial permeability, allowing excessive enzyme loss to the aqueous humor. Domestic chicks reared under continuous light (24L/0D) develop severe morphologic and physi-ologic ocular lesions which culminate in glaucoma and blindness. We have called the condition light-induced avian glaucoma. Although human open-angle glaucoma is a serious clinical problem, few experimental animals develop such a disease and in no others, to our knowledge, can the condition be precipitated at the will of the investigator. Light-induced avian glaucoma is associated with increased eye weight and diameter, reduced cor-neal curvature, impaired outflow facility, and elevated intraocular (IOP) pressure. 1 '-Eye enlargement and refractive error are detectable several weeks before outflow facility is impaired, and IOP is elevated still later in the disease process. 8 Although the iridocorneal angle is narrow, iridectomy of chicks, subsequently reared under 24L/0D, failed to alter the course of the developing glaucoma, as might be expected if pupillary block had contributed to iris bombe. 1 A systemic rather than a local etiology was suggested by the finding that eyes of 24L/0D birds, when covered by an opaque vision occluder, showed no less enlargement than those not so covered. 5 However, these positive findings have provided few clues about the etiology of light-induced avian glaucoma. Improvements in our techniques have now made it possible to monitor aqueous fluid dynamics in chicks as young as seven days after hatching: we here detail these early pre-glaucomatous changes. We have also measured …