AN ANIMAL-MODEL OF MYOPIA
AN ANIMAL-MODEL OF MYOPIA
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DOI：
10.1056/nejm198506203122505
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发表时间：
1985-01-01
影响因子：
158.5
通讯作者：
WIESEL, TN
中科院分区：
文献类型：
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作者：
RAVIOLA, E;WIESEL, TN
猕猴在出生时通过手术将眼睑融合，并保持关闭一年，从而形成近视。这种实验性屈光不正与人类近视有许多共同的特征：它是由眼睛的渐进性轴向伸长引起的，通常伴有眼底变化，并且只能在眼睛生长完成之前诱导。在黑暗中饲养的动物不会产生近视;因此，它是由视觉输入的改变触发的，并且可能是由神经系统介导的。在猕猴中，阿托品可防止眼球异常伸长，这表明眼睑融合性近视是由过度调节引起的。InM.因此，阿托品是无效的;此外，当在中断视路后缝合眼睑时，会发生近视。因此，在这个物种中，调节可以被排除作为眼睛伸长的决定因素，其他神经机制可能是导致屈光不正的原因。我们的实验表明，屈光状态在很大程度上是在遗传基础上编程的，但是异常的视觉体验会破坏出生后眼睛生长的过程并诱导轴性近视。（N Engl J Med 1985; 312：1609-15.）
Myopia develops in macaque monkeys when their lids are surgically fused at birth and kept closed for one year. This experimental refractive error has many features in common with human myopia: It is caused by progressive axial elongation of the eye, is often accompanied by fundus changes, and can only be induced before eye growth has been completed. Myopia does not develop in animals raised in the dark; thus, it is triggered by an alteration of the visual input and is presumably mediated by the nervous system. InMacaca arctoides,atropine administration prevents abnormal eye elongation, and this suggests that lid-fusion myopia is caused by excessive accommodation. InM. mulatta,atropine is ineffective; furthermore, myopia develops when lids are sutured after interruption of the optic pathways. Thus, in this species accommodation can be ruled out as a determinant of eye elongation, and other neural mechanisms may be responsible for the refractive error. Our experiments suggest that the refractive state is largely programmed on a genetic basis, but that an abnormal visual experience can disrupt the process of postnatal eye growth and induce axial myopia. (N Engl J Med 1985; 312:1609–15.)