Diurnal fluctuations and developmental changes in ocular dimensions and optical aberrations in young chicks

PURPOSE: To investigate further the emmetropization process in young chicks by studying the diurnal fluctuations and developmental changes in the ocular dimensions and optical aberrations, including refractive errors, of normal eyes and eyes that had the ciliary nerve sectioned (CNX). METHODS: The ocular dimensions and aberrations in both eyes of eight CNX (surgery on right eyes only) and eight normal chicks were measured with high-frequency A-scan ultrasonography and aberrometry, respectively, four times a day on five different days from posthatching day 13 to 35. A fixed pupil size of 2 mm was used to analyze aberration data. Repeated-measures ANOVA was applied to examine the effects of age, time of day, and surgery. RESULTS: Refractive errors and most higher-order aberrations decreased with development in both normal and CNX eyes. However, although normal eyes showed a positive shift in spherical aberration with age, changing from negative spherical aberration initially, CNX eyes consistently exhibited positive spherical aberration. Anterior chamber depth, lens thickness, vitreous chamber depth, and thus optical axial length all increased with development. Many of these ocular parameters also underwent diurnal changes, and mostly these dynamic characteristics showed no age dependency and no effect of CNX. Anterior chamber depth, vitreous chamber depth, and optical axial length were all greater in the evening than in the morning, whereas the choroids were thinner in the evening. Paradoxically, eyes were more hyperopic in the evening, when they were longest. Although CNX eyes, having enlarged pupils, were exposed to larger higher-order aberrations, their growth pattern was similar to that of normal eyes. CONCLUSIONS: Young chicks that are still emmetropizing, show significant diurnal fluctuations in ocular dimensions and some optical aberrations, superimposed on overall increases in the former and developmental decreases in the latter, even when accommodation is prevented. The possibility that these diurnal fluctuations are used to decode the eye's refractive error status for emmetropization warrants investigation. That eyes undergoing ciliary nerve section have more higher-order aberrations but do not become myopic implies a threshold for retinal image degradation below which the emmetropization process is not affected.     

Elevated dark-adapted thresholds in albino rodents

Albino mice and rats have elevated dark-adapted thresholds compared to normally pigmented animals. The absolute dark-adapted incremental threshold for black mice is about 1.5 log units lower than the threshold for albino mice when measured by single-unit recordings from the superior colliculus. Cell counts from the outer nuclear layer in albino mice are not significantly different from those in black mice, indicating that the elevated dark-adapted thresholds are not due to light damage of photoreceptor cells. No photoreceptor outer segment damage was found in these albino animals at the light or electron microscopic level. These experiments have been repeated in hooded and albino rats. The thresholds from albino rats were about 2 log units higher than the thresholds from pigmented rats in the dark-adapted state. The proximity of the retinal pigment epithelium (RPE) and the pigmented choroid to the photoreceptors in these animals suggests that a reduction in ocular melanin in hypopigmented animals may be causal to their elevated thresholds.     

Effects of optical defocus and spatial contrast on anterior chamber depth in chicks

The goal of this study was to investigate the effect of optical defocus and spatial contrast on refractive development and, in particular,on anterior chamber growth. Ninety chicks were raised from day 4-10 post-hatching wearing monocular lenses (+/-10 Dor 0 D), in an environment with either high, low or no spatial contrast patterns: 30%, 6% or 0% contrast, respectively. At day 10, the chicks' refractive state and ocular components were assessed using retinoscopy and A-scan ultrasonography. Ocular defocus resulted in sign-dependent significant differences in refractive error, axial length and vitreous chamber depth. Lens wear also led to significant spatial contrast dependent changes in anterior chamber depth. Varying ambient spatial contrast in the chick's environment did not inhibit emmetropization processes; however, anterior chamber growth was particularly susceptible to changes in spatial contrast.     

The role of ocular pigmentation in protecting against retinal light damage

Albino and pigmented rats exposed to similar constant light conditions were compared in terms of their susceptibility to retinal damage. Pigmented rats showed considerable resistance to light damage but, when their pupils were maximally dilated, they damaged only about twice as slowly as albinos. When compared at light intensities that caused equal steady-state rhodopsin bleaches, albino and dilated pigmented rats showed essentially the same rate of light-induced retinal degeneration. These experiments suggest that the inherent susceptibility of the retina to light damage is about the same in albino and pigmented rats and that ocular pigmentation protects against damage primarily by lowering the retinal irradiance.     

Albinism: its implications for refractive development

PURPOSE: Albinism involves the mutation of one or more of the genes associated with melanin synthesis and has many ramifications for vision. This study focuses on the refractive implications of albinism in the context of emmetropization. METHODS: Refractive, biometric, and visual acuity data were collected for a group of 25 albino individuals that included the following: 18 oculocutaneous (13 tyrosine positive, 5 tyrosine negative); 7 ocular (2 autosomal recessive, 5 sex-linked recessive). Their age range was 3 to 51 years. All exhibited horizontal pendular nystagmus. RESULTS: There were no statistically significant differences relating to albino subtype for any of the measured parameters. All the subjects had reduced visual acuity (mean: 0.90, logMAR) and overall, there was a bias toward hyperopia in their refractive errors (mean: + 1.07 D). However the refractive errors of the group covered a broad range (SD: 4.67 D) and included both high myopia and high hyperopia. An axial origin to the refractive errors is implied by the high correlation between refractive errors and axial lengths. Refractive astigmatism averaged 2.37 D and was consistently with-the-rule and highly correlated with corneal astigmatism, which was also with-the-rule. Meridional analysis of the refractive data indicated that the vertical meridian for hyperopic subjects was consistently nearer emmetropia compared to their horizontal meridian. Myopic subjects showed the opposite trend. CONCLUSIONS: The overall refractive profile of the subjects is consistent with emmetropization being impaired in albinism. However, the refractive errors of hyperopic subjects also can be explained in terms of "meridional emmetropization." The contrasting refractive profiles of myopic subjects may reflect operational constraints of the emmetropization process.     

The significance of retinal image contrast and spatial frequency composition for eye growth modulation in young chicks

PURPOSE: This study sought further insight into the stimulus dependence of form deprivation myopia, a common response to retinal image degradation in young animals. METHODS: Each of 4 Bangerter diffusing filters (0.6, 0.1, <0.1, and LP (light perception only)) combined with clear plano lenses, as well as plano lenses alone, were fitted monocularly to 4-day-old chicks. Axial ocular dimensions and refractive errors were monitored over a 14-day treatment period, using high frequency A-scan ultrasonography and an autorefractor, respectively. RESULTS: Only the <0.1 and LP filters induced significant form deprivation myopia; these filters induced similarly large myopic shifts in refractive error (mean interocular differences+/-SEM: -9.92+/-1.99, -7.26+/-1.60 D, respectively), coupled to significant increases in both vitreous chamber depths and optical axial lengths (p<0.001). The other 3 groups showed comparable, small changes in their ocular dimensions (p>0.05), and only small myopic shifts in refraction (<3.00 D). The myopia-inducing filters eliminated mid-and-high spatial frequency information. CONCLUSIONS: Our results are consistent with emmetropization being tuned to mid-spatial frequencies. They also imply that form deprivation is not a graded phenomenon.     

The role of the retinal pigment epithelium in eye growth regulation and myopia: a review

Myopia is increasing in prevalence world-wide, nearing epidemic proportions in some populations. This has led to expanded research efforts to understand how ocular growth and refractive errors are regulated. Eye growth is sensitive to visual experience, and is altered by both form deprivation and optical defocus. In these cases, the primary targets of growth regulation are the choroidal and scleral layers of the eye that demarcate the boundary of the posterior vitreous chamber. Of significance to this review are observations of local growth modulation that imply that the neural retina itself must be the source of growth-regulating signals. Thus the retinal pigment epithelium (RPE), interposed between the retina and the choroid, is likely to play a critical role in relaying retinal growth signals to the choroid and sclera. This review describes the ion transporters and signal receptors found in the chick RPE and their possible roles in visually driven changes in eye growth. We focus on the effects of four signaling molecules, otherwise implicated in eye growth changes (dopamine, acetylcholine, vasoactive intestinal peptide (VIP), and glucagon), on RPE physiology, including fluid transport. A model for RPE-mediated growth regulation is proposed.     

Congenital simple hamartoma of the retinal pigment epithelium: a study of five cases

PURPOSE: To report 5 patients with presumed congenital, simple hamartoma of the retinal pigment epithelium (RPE). DESIGN: Retrospective, observational small case series. PARTICIPANTS: Five patients with a black macular tumor of the RPE. MAIN OUTCOME MEASURES: Initial tumor features, initial associated fundus features, tumor course on follow-up, and visual acuity outcome. RESULTS: In all 5 cases, the tumor involved the macula and the mean distance to the foveola was 0.4 mm (median, 0.2 mm; range, 0.2-1.2 mm). In all cases, the tumor was darkly pigmented, with full-thickness retinal and RPE involvement and minimal protrusion into the vitreous cavity. The mean ultrasonographic tumor thickness was 1.6 mm (median, 1.4 mm; range, 1.1-2.5 mm). Associated features included minimally dilated retinal feeding artery and draining vein (100%), surrounding mild retinal traction (80%), retinal exudation (20%), and vitreous pigmented cells (20%). None of the lesions had associated subretinal fluid, macular edema, or macular hole. Visual acuity was 20/20 in 3 cases and slightly decreased in the other 2 cases because of foveal traction. The findings remained stable in 3 patients who had adequate follow-up. We chose to classify this lesion as congenital simple hamartoma of the RPE to differentiate it from combined hamartoma of the retina and RPE, congenital hypertrophy of the RPE, adenoma or adenocarcinoma of the RPE, and acquired hyperplasia of the RPE, which are different clinical entities. CONCLUSIONS: Congenital hamartoma of the RPE is typically a black, full-thickness retinal mass, often adjacent to the foveola. Despite such location, the visual acuity was affected minimally.     

Heritability of ocular component dimensions in chickens: genetic variants controlling susceptibility to experimentally induced myopia and pretreatment eye size are distinct

Purpose. To investigate the extent to which shared genetic variants control (1) multiple ocular component dimensions and (2) both normal eye length and susceptibility to visually induced myopic eye growth. Methods. Two laboratory-reared populations of chicks were examined. The first was a three-generation pedigree of White Leghorn (WL) birds used in a selective breeding experiment testing susceptibility to monocular deprivation of sharp vision (DSV). The chicks were assessed before (age, 4 days) and after 4 days of treatment with diffusers. The second was the 10th generation of an advanced intercross line (AIL) derived from a broiler-layer cross (age, 3 weeks). Variance components analysis was used to estimate heritability and to assess the evidence for shared genetic determination. Results. All measured ocular components were moderately or highly heritable (range, 0.36-0.61; all P < 0.001) in both chick populations, and there were strong genetic correlations across the traits, corneal curvature, vitreous chamber depth, and axial length. The genetic correlations between eye size and myopia susceptibility traits were not significantly different from 0. Conclusions. The genetic variants controlling ocular component dimensions in chicks are shared across some ocular traits (corneal curvature, vitreous chamber depth, and axial length) but distinct for others (lens thickness and corneal thickness). The genetic variants controlling susceptibility to visually induced myopia in chicks are different from those controlling normal eye size.     

Ultrastructural localization of lipid peroxides as benzidine-reactive substances in the albino mouse eye

· Background: Lipid peroxidation is considered to be a prominent feature of retinal degeneration and has also been proposed to be involved in the pathogenesis of age-related macular degeneration. Melanin protects against lipid peroxidation and takes part in the detoxification of lipid peroxides (LP). LP can be ultrastructurally detected as benzidine-reactive substances (BRS) using tetramethylbenzidine (TMB). Albino mice lack melanin. In the present study, LP were localized as BRS in the eyes of albino and pigmented mice. · Methods: Eye cups of an albino mouse lineage and of wild-type mice were fixed with 2% glutaraldehyde, incubated with 0.5 mg/ml TMB and embedded for electron microscopy. · Results: BRS were detected in the eyes of albino mice, but no reaction product was seen in pigmented eyes. BRS located in the retinal pigment epithelium (RPE) and in the choroid of the albino mouse; no BRS were found in intact rod outer segments (ROS). · Conclusion: The lack of melanin in albino mice is associated with a higher level of lipid peroxidation in RPE and choroid. Melanin seems to protect against LP in RPE and choroid. A lack of melanin is not associated with lipid peroxidation in intact ROS. The present investigation demonstrates the significance of melanin in protection against LP in RPE and choroid. Received: 16 November 1998 Revised version received: 18 January 1999 Accepted: 19 January 1999     

Relative afferent pupillary defect in the "better" eye

A relative afferent pupillary defect usually occurs in an eye with unilateral or asymmetric optic nerve or extensive retinal disease. In general, the eye with poorer visual acuity has the afferent pupillary defect. Twenty-five patients are reported, however, in whom an afferent pupillary defect occurred in the eye with better visual acuity. These eyes had optic nerve or retinal dysfunction. The eyes with worse visual acuity but no afferent pupillary defect had an abnormality of the ocular media (corneal opacity, hyphema, anterior segment membrane, cataract, or vitreous opacity), amblyopia, refractive error, age-related macular degeneration, or cystoid macular edema. An afferent pupillary defect does not necessarily occur in the eye with poorer visual acuity.     

Axial growth and changes in lenticular and corneal power during emmetropization in infants

PURPOSE: To evaluate the contribution made by the ocular components to the emmetropization of spherical equivalent refractive error in human infants between 3 and 9 months of age. METHODS: Keratophakometry in two meridians was performed on 222 normal-birthweight infant subjects at 3 and 9 months of age. The spherical equivalent refractive error was measured by cycloplegic retinoscopy (cyclopentolate 1%). Anterior chamber depth, lens thickness, and vitreous chamber depth were measured by A-scan ultrasonography over the closed eyelid. RESULTS: Both the mean and SD for spherical equivalent refractive error decreased between 3 and 9 months of age (+2.16 +/- 1.30 D at 3 months; +1.36 +/- 1.06 D at 9 months; P < 0.0001, for the change in both mean and SD). Average ocular component change was characterized by increases in axial length, thinning, and flattening of the crystalline lens, increases in lens equivalent refractive index, and decreases in lens and corneal power. Initial refractive error was associated in a nonlinear manner with the change in refractive error (R(2) = 0.41; P < 0.0001) and with axial growth (R(2) = 0.082; P = 0.0005). Reduction in hyperopia correlated significantly with increases in axial length (R(2) = 0.16; P < 0.0001), but not with changes in corneal and lenticular power. Decreases in lenticular and corneal power were associated with axial elongation (R(2) = 0.40, R(2) = 0.12, respectively; both P < 0.0001). CONCLUSIONS: Modulation in the amount of axial growth in relation to initial refractive error appeared to be the most influential factor in emmetropization of spherical equivalent refractive error. The associations between initial refractive error, subsequent axial growth, and change in refractive error were consistent with a visual basis for emmetropization. The cornea and crystalline lens lost substantial amounts of dioptric power in this phase of growth, but neither appeared to play a significant role in emmetropization.     

Constant light rearing disrupts compensation to imposed- but not induced-hyperopia and facilitates compensation to imposed myopia in chicks

PURPOSE: While rearing chicks in constant light (CL) inhibits anterior segment growth, these conditions also induce excessive enlargement of the vitreous chamber. The mechanisms underlying these effects are poorly understood although it has been speculated that the enlarged vitreous chambers are a product of emmetropization, a compensatory response to the altered anterior segments. We examined the ability of eyes to compensate to defocusing lenses in CL as a direct test of their ability to emmetropize. We also studied recovery responses, i.e. from lens-induced changes in CL as well as CL-induced changes alone or combined with lens-induced changes in eyes returned to normal diurnal lighting (NL). METHODS: Hatchling White-Leghorn chicks were reared in either CL or NL (control) lighting conditions (n=36) for 2 weeks, with lenses of either +10 or -10D power fitted to one eye of all chicks at the beginning of the second week. The lenses were removed at the end of the same week, at which time some CL chicks (n=14) were shifted to NL, the rest of the chicks remaining in their respective original lighting conditions. Retinoscopy, IR photo-keratometry and high-frequency A-scan ultrasonography were used to track refractions, corneal radii of curvature and ocular axial dimensions, respectively; data were collected on experimental days 0, 7, 9, 14 and 21. RESULTS: Under CL, eyes showed near normal, albeit slightly exaggerated responses to +10D lenses while the response to -10D lenses was disrupted. With +10D lenses, lens-wearing eyes became more hyperopic (RE), and had shorter vitreous chambers (VC) and optical axial lengths (OL) relative to their fellows by the end of the lens period [RE: +10.5+/-1.5D, CL, +8.25+/-2.5D, NL; VC: -0.363+/-0.129mm, CL; -0.306+/-0.110mm, NL; OL: -0.493+/-0.115mm, CL, -0.379+/-0.106mm, NL (mean interocular difference+/-SD)]. With -10D lenses, the NL group showed a myopic shift in RE and increased elongation of both VC depth and OL (RE: -10.75+/-2.0D; VC depth: 0.554+/-0.097mm; OL: 0.746+/-0.166mm), while the CL group showed a small hyperopic shift in RE (+4.0+/-6.0D). Nonetheless, CL eyes were able to recover from lens-induced hyperopia, whether they were left in CL or returned to NL. One week of exposure to NL was sufficient to reverse the effects of 2 weeks of CL on anterior and vitreous chamber dimensions. CONCLUSION: CL impairs emmetropization. Specifically, it disrupts compensation to lens-imposed hyperopia but not imposed myopia. However, CL eyes are able to recover from lens-induced hyperopia, suggesting that the mechanisms underlying the compensatory responses to defocusing lenses are different from those involved in recovery responses. The ocular growth effects of CL on young eyes are reversible under NL.     

Bidirectional, Optical Sign-Dependent Regulation of BMP2 Gene Expression in Chick Retinal Pigment Epithelium

Purpose. We explored the role of bone morphogenic protein 2 (BMP2) in defocus-induced ocular growth using gene expression changes in RPE as a surrogate. Methods. Young White-Leghorn chickens were used in this study. Normal gene expression of BMP2 and its receptors was examined in retina, RPE, and choroid, and BMP2 protein expression assessed in the same tissues using Western blots and immunohistochemistry. Quantitative PCR (qPCR) was used to assess the effects of short-term exposure (2 or 48 hours) to monocular +10 and -10 diopter (D) lenses, on RPE gene expression of BMP2 and its receptors. Ocular growth was assessed using A-scan ultrasonography. Results. In the eyes of untreated chickens, BMP2 mRNA was expressed more highly in RPE compared to retina and choroid and all three tissues expressed BMP2 protein. The gene expression for all three receptors also was detected in these tissues, with BMPR2 showing highest and BMPR1B lowest expression. BMP2 was up-regulated in the RPE from eyes wearing +10 D lenses, which exhibited shorter than normal vitreous chambers (VCDs) and thickened choroids, while BMP2 was down-regulated in the RPE from eyes wearing -10 D lenses, which developed enlarged VCDs. These treatments did not induce differential expression of BMP receptors in RPE. Conclusions. That mRNA expression of BMP2 in chick RPE shows bidirectional, defocus sign-dependent changes is suggestive of a role for BMP2 in eye growth regulation, although the diffuse ocular expression of BMP2 and its receptors suggests complex growth-modulatory signal pathways.     

Herpes simplex virus mediated gene transfer to primate ocular tissues.

We evaluated the feasibility of delivering a gene into monkey eyes using a replication-competent herpes simplex virus (HSV) type 1 ribonucleotide reductase mutant (hrR3) expressing the Escherichia coli lacZ gene. To determine the efficiency of in vitro HSV-mediated gene transfer, cultured human trabecular meshwork (HTM) and human ciliary muscle (HCM) cells were infected with hrR3 and beta-galactosidase activity was measured histochemically. Six cynomolgus monkey eyes received viral injections into the anterior chamber (2 x 10(7) pfu) and/or the vitreous (5 x 10(7) pfu), and the distribution of cells expressing lacZ was evaluated. In vitro, both cultured HTM and HCM cells displayed multiplicity-dependent beta-galactosidase activity. In vivo, intracameral and/or intravitreal injection resulted in transgene expression in TM cells and in non-pigmented ciliary epithelial cells (NPE), but not in CM cells. Transgene expression was also detected in retinal pigmented epithelial (RPE) cells and sporadic retinal ganglion cells (RGC) in eyes receiving virus intracamerally and intravitreally respectively. We observed significant inflammation in the anterior chamber, TM and CM in virus-injected eyes, along with mild vitritis and retinitis. This study demonstrates successful gene transfer using hrR3 as a vector in human ocular cells and in ocular tissues in living monkeys. Further investigation of the etiology of the inflammatory response, possible cytotoxicity, and limited duration of transgene expression is necessary in order to make this technique clinically applicable.     

The sensitivity of the chick eye to refractive defocus

The chick is commonly used as an animal model for human myopia and emmetropization. However one criticism of this model has been the very large refractive errors that are usually induced, either by visual deprivation or through the use of lenses to first impose focussing errors This study sought to determine the threshold for compensatory responses to imposed defocus. We observed compensation in chick eyes fitted at hatching with +1 D and −1 D lenses (one over each eye). Consistent with the 2D interocular difference in refraction imposed, an average of 2.130 (SD 1.0D) of anisometropia and a 0.09mm (SD 0.05mm) interocular difference in vitreous chamber depth were recorded after five days of lens wear. The 1 D focusing errors imposed on individual eyes are not much greater in magnitude than the estimated depth of focus of the chick eye. The significance of these results for emmetropization are discussed.     

准分子激光角膜切削术性光学离焦对幼猴正视化影响的研究

目的了解视觉反馈对幼猴正视化过程的调控作用。方法年龄2～3个月的健康恒河猴8只,每只猴一只眼接受准分子激光角膜屈光手术(PRK),使术后产生3．0O D相对近视或远视性离焦(各4只);另一只眼作为对照。术后不同时间用角膜地形图、散瞳验光、A超和裂隙灯显微镜动态观察猴眼的变化。结果术眼角膜上皮均在术后3d之内完全愈合,在观察期内角膜保持透明。实验眼均表现为代偿生长的过程,玻璃体腔增长速率随术后屈光状态不同而变化。术后远视性离焦,玻璃体腔增长速率较对照眼快(t=3．656,P=0．0354);术后近视性离焦,玻璃体腔增长速率较对照眼慢(t=3．576,P=0．0374)。结论PRK造成光学离焦,可以调控幼猴的玻璃体腔生长和正视化过程,表明幼猴的正视化过程受视觉反馈的调节,提示临床上婴幼儿屈光不正的光学矫正应慎重。PRK造成猴眼光学离焦动物模型可用于视觉科学的研究。     

The regulation of eye growth and refractive state: an experimental study of emmetropization

During growth the vertebrate eye achieves a close match between the power of its optics and its axial length with the result that images are focused on the retina without accommodative effort (emmetropia). The possibility that vision is required for the regulation of eye growth was studied experimentally in chicks made myopic or hyperopic by different visual manipulations. After discontinuing these visual manipulations, the eyes returned quickly to emmetropia mainly by adjusting the growth of their vitreous chambers; growth stopped in eyes recovering from myopia and continued in eyes recovering from hyperopia. Because both hyperopic and myopic eyes were already larger than normal controls, the difference in growth indicates that refractive error, rather than eye size per se, guides the eye toward emmetropia. Evidence is also presented for nonvisual shape-related control of eye growth, but this is slow-acting and cannot explain the emmetropization from induced refractive errors. Both the visually guided and shape-related mechanisms work even in eyes with the optic nerve cut, indicating that the two mechanisms are local to the eye. Although the optic-nerve-sectioned eye can sense the sign of a refractive error and initially adjust growth accordingly, it eventually overshoots emmetropia and reverses the sign of the initial refractive error. Whether this is due to loss of feedback from the central nervous system or retinal ganglion cells is unclear.     

Patching fellow eyes during subjective night does not prevent disruption to minus lens compensation in constant light-reared chicks

PURPOSE: This study re-examined an earlier claim that monocular patching during subjective night (i.e. patched at the usual time that night would occur) in the chicks reared in continuous lighting (CL), offered unpatched eyes some protection from the ocular effects of CL. It also examined whether this monocular patching protected unpatched eyes against the disruptive effect of CL on compensation to minus lenses. METHODS: Hatchling White-Leghorn chicks were reared in either constant or diurnal lighting conditions (n=28) for 2 weeks. Some CL chicks had their right eyes patched every night during the entire study. Lenses of either +10 or -10D power were fitted to the unpatched eyes of some patched chicks at the beginning of the second week. Retinoscopy, IR photo-keratometry and high-frequency A-scan ultrasonography were used to track refractions, corneal radius of curvature and ocular axial dimensions respectively; data were collected on experimental days 0, 7, 9 and 14. RESULTS: The patched eyes were completely protected from the ocular growth effects of CL, i.e. accelerated posterior segment (vitreous chamber) growth and inhibited anterior segment growth. Although the unpatched eyes showed no protection from the anterior chamber effects of CL, they were completely protected from the effects of CL on vitreous chamber growth. Nonetheless, the response to the -10D lenses was disrupted in unpatched eyes, which responded in the wrong direction for compensation (+5.5+/-0.25D more hyperopic than no lens-unpatched eyes). The response to the +10D lenses was preserved (+9.25+/-0.25D more hyperopic than no lens-unpatched eyes). CONCLUSION: These data provide further support for local control of emmetropization, as reflected in compensatory lens responses, but point to additional influences on eye growth as reflected in CL-induced ocular changes.     

姜黄素防治兔眼增生性玻璃体视网膜病变的实验研究

背景先前的系列研究表明,姜黄素可以诱导体外培养的兔视网膜色素上皮（RPE）细胞凋亡,抑制其RPE细胞的增生,且在玻璃体内应用后不良反应较小,具有防治增生性玻璃体视网膜病变（PVR）的潜在价值。目的探讨姜黄素玻璃体内注射对RPE细胞诱导的兔眼PVR模型的防治效果。方法新西兰白兔20只40只眼,所有兔眼玻璃体注射前先抽取0．2ml玻璃体液,然后在兔眼玻璃体内注射0．1ml（2×10^6）同种RPE细胞,每只兔随机选取1只眼立即注入1mg／L的姜黄素0．1ml作为姜黄素组（20只眼）,对侧眼注入等量的含质量分数0．5‰DMSO的生理盐水作为对照组（20只眼）。注药后1、3、7、14、21、28d裂隙灯显微镜下观察角膜、房水、晶状体的透明度及眼前节炎症反应情况;使用间接检眼镜、眼底彩色照相和B型超声检查玻璃体视网膜情况。以视网膜脱离发生眼数作为检测指标,评价姜黄素对PVR的防治效果。结果玻璃体注药后1d、3d所有兔眼发生眼前节炎症反应,玻璃体轻中度混浊,但未见增生条带及视网膜脱离。玻璃体注药后7d,所有兔眼前节炎症反应基本消退,对照组14只眼（75％）玻璃体出现增生条带,姜黄素组2只眼（10％）玻璃体内出现增生条带,差异有统计学意义（P〈0．01）,但2组均未见视网膜脱离。注药后14d,对照组11只眼（55％）出现视网膜脱离,姜黄素组2只眼（10％）出现视网膜脱离,差异有统计学意义（P〈0．01）;注药后21d,对照组16只眼（80％）出现视网膜脱离,姜黄素组3只眼（15％）出现视网膜脱离;注药后28d,对照组19只眼（95％）出现视网膜脱离,姜黄素组3只眼（15％）出现视网膜脱离,差异有统计学意义（P〈0．01）。结论姜黄素玻璃体腔内注射可以有效预防RPE细胞诱导的兔眼实验性PVR的发生发展。