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眼组织对急性压力诱导缺血的敏感性。

Sensitivities of ocular tissues to acute pressure-induced ischemia.

作者信息

Anderson D R, Davis E B

出版信息

Arch Ophthalmol. 1975 Apr;93(4):267-74. doi: 10.1001/archopht.1975.01010020277006.

Abstract

Intraocular pressure was artificially elevated for eight hours in eight owl monkeys. The first permanent effect (produced at a perfusion pressure of plus 15 mm Hg) was partial necrosis of iris stroma and ciliary processes, associated with microscopic lesions in the photoreceptors and retina pigment epithelium around the disc and in the retinal periphery. At a slightly higher pressure, visual nerve fibers in the retina and optic nerve and their ganglion cells were affected. Simultaneously, the outer retinal layers showed damage to the pigment epithelium, photoreceptors, and other nuclear layers. At even higher pressures, nearly all the other intraocular tissues were affected except for Müller cells, astroglia in the optic nerve head, epithelium of the pars plana, and the pigment cells of the choroid. The possibility is raised of a nonischemic pressure-induced mechanism for destruction of disc astrocytes in human chronic glaucoma.

摘要

在八只猫头鹰猴身上将眼压人为升高八小时。第一个永久性效应(在灌注压为+15毫米汞柱时产生)是虹膜基质和睫状体的部分坏死,伴有视盘周围及视网膜周边的光感受器和视网膜色素上皮的微观病变。在稍高的压力下,视网膜和视神经中的视觉神经纤维及其神经节细胞会受到影响。同时,视网膜外层显示色素上皮、光感受器和其他核层受损。在更高的压力下,除了米勒细胞、视神经乳头中的星形胶质细胞、扁平部上皮和脉络膜色素细胞外,几乎所有其他眼内组织都会受到影响。这就提出了一种在人类慢性青光眼中非缺血性压力诱导机制破坏视盘星形胶质细胞的可能性。

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