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光对大鼠模型中氧诱导性视网膜病变的影响。大鼠中的光与氧诱导性视网膜病变。

Effect of light on oxygen-induced retinopathy in the rat model. Light and OIR in the rat.

作者信息

Ricci B, Lepore D, Iossa M, Santo A, D'Urso M, Maggiano N

机构信息

Department of Ophthalmology, Catholic University, Rome, Italy.

出版信息

Doc Ophthalmol. 1990 Apr-Jul;74(4):287-301. doi: 10.1007/BF00145813.

DOI:10.1007/BF00145813
PMID:1701697
Abstract

The purpose of this study was to establish whether exposure to intense lighting favors the development or aggravates experimental oxygen-induced retinopathy in the newborn rat. Five groups of Wistar rats were studied. The control group was maintained for the first 14 days of life under conditions of cyclical (12L:12D) lighting at 12 Lx in room air. Two other groups were subjected, for the same amount of time, to semi-darkness (2 Lx; 12L: 12D), one with room air and the other with supplemental 80% oxygen. The final two groups were exposed to the same room air and hyperoxic treatments under intense lighting conditions (600 Lx; 12L:12D). After the treatment period, four rats were randomly chosen from each group, sacrificed and their retinas examined under electron microscope. Marked structural changes were seen only in the photoreceptor outer segments of those rats exposed to intense light. In eighty-five of the remaining rats retinal vascular morphology was examined in retinal flat mounts after intracardiac injection of India ink. Retinopathy was observed in rats treated with hyperoxia but no significant differences could be attributed to the light conditions under which the retinopathic rats had been maintained. In the rest of the rats, axonal transport along the optical pathways was evaluated after intravitreal injection of (3H) taurine. In the two groups exposed to hyperoxia, axonal transport was altered, but less markedly in those exposed to intense lighting than in those exposed to semi-darkness. Intense illumination under conditions of normoxia favors axonal transport. Exposure to intense lighting does not seem to aggravate oxygen induced retinopathy in the rat though it does produce structural lesions of the photoreceptors.

摘要

本研究的目的是确定暴露于强光下是否有利于新生大鼠实验性氧诱导视网膜病变的发展或加重其病情。对五组Wistar大鼠进行了研究。对照组在出生后的前14天,饲养于室内空气中,光照为12勒克斯,呈周期性(12小时光照:12小时黑暗)。另外两组在相同时间内处于半暗环境(2勒克斯;12小时光照:12小时黑暗),一组呼吸室内空气,另一组呼吸补充了80%氧气的空气。最后两组在强光条件下(600勒克斯;12小时光照:12小时黑暗)呼吸相同的室内空气并接受高氧处理。治疗期结束后,从每组中随机选取四只大鼠,处死后在电子显微镜下检查其视网膜。仅在暴露于强光的大鼠的光感受器外段观察到明显的结构变化。在其余的85只大鼠中,心内注射印度墨汁后,在视网膜平铺标本中检查视网膜血管形态。在接受高氧治疗的大鼠中观察到视网膜病变,但视网膜病变大鼠所处的光照条件并无显著差异。在其余大鼠中,玻璃体内注射(3H)牛磺酸后,评估沿视觉通路的轴突运输。在两组暴露于高氧的大鼠中,轴突运输发生改变,但暴露于强光下的大鼠的改变程度不如暴露于半暗环境下的大鼠明显。常氧条件下的强光照射有利于轴突运输。暴露于强光下似乎不会加重大鼠的氧诱导视网膜病变,尽管它确实会导致光感受器的结构损伤。

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Early light reduction for preventing retinopathy of prematurity in very low birth weight infants.早期减少光照预防极低出生体重儿早产儿视网膜病变

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