Zhong Xingwu, Ge Jian, Nie Haohui, Chen Xiaolian, Huang Juan, Liu Nian
Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Peoples Republic of China.
Invest Ophthalmol Vis Sci. 2004 Oct;45(10):3806-11. doi: 10.1167/iovs.03-0326.
To investigate whether photorefractive keratectomy (PRK) performed in infant primates can modify emmetropization and therefore could be used to study mechanisms of refractive error development.
Six healthy rhesus monkeys ranging in age from 2 to 3 months were randomly divided into two groups (n = 3 each). Anisometropia was induced in each animal by performing PRK on one eye. Hyperopic anisometropia was induced in group A monkeys by flattening the cornea of the right eye, whereas myopic anisometropia was produced in group B monkeys by steepening the cornea of the right eye. Corneal morphology and topography, refractive status, and axial growth were evaluated over a 5-month observation period.
All the PRK-treated corneas were re-epithelialized and transparent within 3 days after surgery. Subsequently, all the surgically treated eyes exhibited interocular alterations in axial growth rate that were appropriate to compensate for the PRK-induced anisometropia. Specifically, vitreous chamber elongation rates were faster in the eyes with induced hyperopias than in their fellow eyes (0.63 +/- 0.05 mm vs. 0.40 +/- 0.09 mm), but slower in the eyes with induced myopia than in their fellow eyes (0.58 +/- 0.13 mm vs. 0.73 +/-0.10 mm). In some animals, the recovery from the induced anisometropia was facilitated by interocular differences in the rate of corneal flattening. However, the rates of corneal flattening in the treated eyes and their fellow eyes were not significantly different.
PRK-induced defocus predictably alters axial growth rate and the normal course of emmetropization in developing eyes. Thus, PRK is a useful alternative to current methods used to impose experimental refractive errors in laboratory animals. These results also indicate that refractive surgery performed in childhood may affect normal growth of the eye, resulting in decreased predictability of future refractive status.
研究在幼年灵长类动物中进行的准分子激光角膜切削术（PRK）是否能改变正视化过程，从而可用于研究屈光不正发展的机制。
将6只年龄在2至3个月的健康恒河猴随机分为两组（每组n = 3）。通过对每只动物的一只眼睛进行PRK诱导产生屈光参差。A组猴子通过 flattening右眼角膜诱导远视性屈光参差，而B组猴子通过 steepening右眼角膜产生近视性屈光参差。在5个月的观察期内评估角膜形态和地形图、屈光状态及眼轴生长情况。
所有接受PRK治疗的角膜在术后3天内重新上皮化且保持透明。随后，所有接受手术治疗的眼睛在眼轴生长速率上均出现了眼间改变，以补偿PRK诱导的屈光参差。具体而言，诱导远视的眼睛玻璃体腔伸长率比其对侧眼更快（0.63 ± 0.05毫米对0.40 ± 0.09毫米），但诱导近视的眼睛玻璃体腔伸长率比其对侧眼更慢（0.58 ± 0.13毫米对0.73 ± 0.10毫米）。在一些动物中，诱导的屈光参差的恢复因角膜 flattening速率的眼间差异而得到促进。然而，治疗眼及其对侧眼的角膜 flattening速率并无显著差异。
PRK诱导的离焦可预测地改变发育中眼睛的眼轴生长速率和正视化的正常进程。因此，PRK是在实验动物中施加实验性屈光不正的现有方法的一种有用替代方法。这些结果还表明，儿童期进行的屈光手术可能会影响眼睛的正常生长，导致未来屈光状态的可预测性降低。
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