Siegwart John T, Norton Thomas T
Department of Vision Sciences, School of Optometry, University of Alabama at Birmingham, Birmingham, Alabama 35294-4390, USA.
Optom Vis Sci. 2013 Feb;90(2):131-9. doi: 10.1097/OPX.0b013e31827cda85.
To determine if early restraint of axial elongation in response to plus lenses increases the subsequent response to interrupted hyperopia in tree shrews.
The normal interrupted hyperopia group (n = 5) had normal visual exposure until 24 days of visual experience (VE). Then, from 24 to 45 days of VE, the animals wore binocular -4-diopter (D) lenses, which shifted the refractive state of the eyes in the direction of hyperopia. Interrupted hyperopia was produced by removing the lenses for 2 hours per day. The early-restraint interrupted hyperopia group (n = 5) wore binocular +4-D lenses continuously from 11 to 24 days of VE, becoming emmetropic with the lenses in place and hyperopic when they were removed. Then, from 24 to 45 days of VE, the lenses were removed 22 hours per day and replaced for 2 hours per day. This created the same initial regimen of interrupted hyperopia as in the normal interrupted hyperopia group. A plus lens control group wore binocular +4-D lenses (n = 5) continuously from 11 to 45 days of VE to assess the stability of the refractive compensation.
In the normal interrupted hyperopia animals, 2 hours of relief from the imposed hyperopia was sufficient to prevent myopia development. In the early-restraint interrupted hyperopia animals, 2 hours of relief from the hyperopia did not prevent myopia development; the eyes became myopic while wearing the lens. The control animals compensated for the +4-D lenses and maintained a stable with-the-lens emmetropia through 45 days of VE, demonstrating that the myopic shift in the early-restraint group was caused by the interrupted hyperopia.
Compensation for plus lenses, involving slowed axial elongation, increases the response to subsequent interrupted hyperopia. Similar to previous reports of an eye size factor in elongated eyes, these data provide evidence for an eye size mechanism operating, in this case, in eyes that have restrained their axial length.
确定对正透镜产生的轴向伸长进行早期抑制是否会增加树鼩随后对间歇性远视的反应。
正常间歇性远视组（n = 5）在视觉经验（VE）24天之前有正常的视觉暴露。然后，从VE 24天到45天，动物佩戴双眼-4屈光度（D）透镜，这使眼睛的屈光状态向远视方向转变。通过每天移除透镜2小时来产生间歇性远视。早期抑制间歇性远视组（n = 5）在VE 11天到24天连续佩戴双眼+4-D透镜，佩戴透镜时变为正视眼，移除透镜时变为远视眼。然后，从VE 24天到45天，每天移除透镜22小时，每天佩戴2小时。这产生了与正常间歇性远视组相同的初始间歇性远视方案。一个正透镜对照组在VE 11天到45天连续佩戴双眼+4-D透镜（n = 5），以评估屈光补偿的稳定性。
在正常间歇性远视动物中，2小时的远视缓解足以防止近视发展。在早期抑制间歇性远视动物中，2小时的远视缓解并不能防止近视发展；眼睛在佩戴透镜时变成了近视眼。对照动物对+4-D透镜进行了补偿，并在45天的VE期间保持了稳定的透镜下正视状态，表明早期抑制组的近视性移位是由间歇性远视引起的。
对正透镜的补偿，包括减缓轴向伸长，增加了对随后间歇性远视的反应。与先前关于长眼眼径因素的报道相似，这些数据为在这种情况下，在轴向长度受到抑制的眼睛中起作用的眼径机制提供了证据。
