Structural and elemental evidence for edema in the retina, retinal pigment epithelium, and choroid during recovery from experimentally induced myopia.
OBJECTIVE
The purpose of this study was to monitor temporal changes in the retina, retinal pigment epithelium (RPE), and choroid of chick eyes using biometric, ultrastructural, and elemental microanalysis techniques as a means of visualizing more detailed signs of the physiological processes underlying choroidal expansion and refractive normalization during recovery from form deprivation.


METHODS
Axial dimensions and refractions were measured on form-deprived and fellow eyes of 117 experimental chickens reared with monocular translucent occlusion from days 1 to 15 and given different lengths of visual experience (T = 0-144 hours) before death. Tissue was analyzed ultrastructurally by electron microscopy and relative sodium (Na) and chloride (Cl) ion abundances, by using x-ray microanalysis to determine changes in the presence of these indicators of tissue hydration.


RESULTS
Refractive error decreased from more than 20 D of myopia almost linearly over the first 144 hours after occlusion. Concurrent changes in thickness in the retina, RPE, and choroid were seen as a series of thickness increases and edema, which returned to normal thickness, first in the retina, and did not reach maximum until 3 days after occluder removal in the choroid. In freeze-dried tissue, Na and Cl ion concentrations were greatest in the RPE photoreceptor outer segments and extravascular choroid at T = 0, decreasing toward fellow eye levels by T = 48 in the RPE and choroid. Na and Cl ion abundances in the frozen lymph of choroidal lymphatics were nearly at control levels (T = 0) and increased later as the vessels became more distended after the extravascular edema became significant.


CONCLUSIONS
The results suggest that occluder removal induces edema across the retina and choroid and that this fluid may be the vector eliciting choroidal expansion during recovery from form deprivation possibly driven by the hyperosmolarity in the choroid, RPE, and photoreceptor outer segments that accompanies deprivation.
Liang
Helena
H
School of Optometry, University of New South Wales, Sydney, New South Wales, Australia.
Crewther
Sheila G
SG
Crewther
David P
DP
Junghans
Barbara M
BM
D000818:Animals; D000831:Animals, Newborn; D002645:Chickens; D002712:Chlorides / Q000378:metabolism; D015862:Choroid Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004577:Electron Probe Microanalysis; D008269:Macular Edema / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D009216:Myopia / Q000150:complications* / Q000503:physiopathology; D010857:Pigment Epithelium of Eye / Q000378:metabolism / Q000648:ultrastructure*; D012160:Retina / Q000378:metabolism / Q000648:ultrastructure*; D012683:Sensory Deprivation; D012964:Sodium / Q000378:metabolism
D002712:Chlorides; D012964:Sodium