Ischemia-reperfusion causes exudative detachment of the rabbit retina.
OBJECTIVE
To characterize the activation of macroglial (Müller) and microglial cells, as well as neuronal cell degeneration, during ischemia-reperfusion in rabbit retina and to test the possible effect of triamcinolone acetonide on gliosis.


METHODS
Transient retinal ischemia was produced by increasing intraocular pressure for 60 minutes. Triamcinolone (8 mg) was intravitreally applied immediately after the cessation of ischemia. At 3 and 8 days after reperfusion, the K+ currents of acutely isolated Müller cells were recorded, and the Ca2+ responses of Müller cells on stimulation of P2Y receptors were recorded fluorometrically in retinal wholemounts. Microglial/immune cells in the nerve fiber layer of retinal wholemounts were labeled with isolectin. To evaluate neuronal and Müller cell loss, the numbers of cells were counted in retinal slices.


RESULTS
Transient ischemia caused exudative detachment of the central retina that was characterized by disruption of the pigment epithelial monolayer, the presence of scattered pigment epithelial and immune cells in the expanded subretinal space, and retinal folds. A significant loss of photoreceptor cells was observed at 8 days after reperfusion. At 3 and 8 days after reperfusion, Müller cell gliosis was apparent, as indicated by cellular hypertrophy, downregulation of K+ channel expression, and an increased number of cells that displayed P2Y receptor-mediated Ca2+ responses. The number of microglial/immune cells increased strongly after reperfusion. Intravitreal triamcinolone did not affect the parameters of Müller cell gliosis but decreased the number of microglial/immune cells.


CONCLUSIONS
Ischemia-reperfusion of the rabbit retina causes exudative retinal detachment that is characterized by a loss of photoreceptor cells, whereas the inner retina remains largely preserved. Micro- and macroglial cells are activated early during reperfusion, even before dropout of the photoreceptor cells. Intravitreal triamcinolone may decrease the degree of microglial/immune cell activation.
Paul Flechsig Institute of Brain Research, University of Leipzig Medical Faculty, Germany.
Ortrud
O
Uckermann
Susann
S
Uhlmann
Thomas
T
Pannicke
Mike
M
Francke
Ruslan
R
Gamsalijew
Felix
F
Makarov
Elke
E
Ulbricht
Peter
P
Wiedemann
Andreas
A
Reichenbach
Neville N
NN
Osborne
Andreas
A
Bringmann
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D002452:Cell Count; D004195:Disease Models, Animal; D005122:Exudates and Transudates; D005260:Female; D005911:Gliosis / Q000188:drug therapy; D005938:Glucocorticoids / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials; D017628:Microglia / Q000378:metabolism / Q000473:pathology; D009412:Nerve Fibers / Q000378:metabolism / Q000473:pathology; D020419:Photoreceptor Cells, Vertebrate / Q000473:pathology; D010857:Pigment Epithelium of Eye / Q000473:pathology; D015221:Potassium Channels / Q000378:metabolism; D011817:Rabbits; D018048:Receptors, Purinergic P2 / Q000378:metabolism; D015427:Reperfusion Injury / Q000150:complications* / Q000473:pathology; D012163:Retinal Detachment / Q000209:etiology* / Q000473:pathology; D012171:Retinal Vessels / Q000473:pathology*; D014222:Triamcinolone Acetonide / Q000494:pharmacology
D015220:Calcium Channels; D005938:Glucocorticoids; D015221:Potassium Channels; D018048:Receptors, Purinergic P2; D014222:Triamcinolone Acetonide