Neuronal Cell Death in Reina Ischemia Induced by Elevation of Intraocular Pressure
Journal of the Korean Ophthalmological Society
; : 2701-2708, 1998.
Article
en Ko
| WPRIM
| ID: wpr-151810
Biblioteca responsable:
WPRO
ABSTRACT
This study was conducted to compare degeneration of retinal neurons in retina ischemia induced by sudden elevation of intraocular pressure(IOP)(Group A) with that by steady elevation of IOP(Group B). Adult male Sprague Dawley rats were used and IOP of 160-180mmHg was maintained for 90 min. Entraocular pressure of 160-180mmHg was achived in a second for Group A, while in one minutes for Group B. The neuronal damage in retina was ascertained by light microscopy and transmission electron microscopy at various time points after ischemic insult. In Group A, retinal neurons were destroyed severely in ganglion cell layer(GCL) and inner nuclear layer(INL) at 24hrs and the number of cells in ganglion cell layer(GCL) was decreased markedly. And some cells in GCL and INL were spread out in inner plexiform layer(IPL) by the 3rd day after ischemia. At each time point, both vecrosis and apoptosis were observed mainly by trasmission electron microscope. In group B, the retinal cell death was observed mainly in ganglion cell layer(GCL) at 24hrs and mainly in inner nuclear layer(INL) of 3 days after ischemia. The characteristics of the retinal injury after 3 days in Group B was similar to that after 24hrs in Group A. Therefore, cell death pattern was delayed in Group B compared with in Group A. With these results It was found that apoptosis as aell as necrosis of the retinal neurons were observed in retina ischemia induced by elevation of IOP cause faster neronal damage than slow elevation of IOP.
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Texto completo:
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Índice:
WPRIM
Asunto principal:
Retina
/
Retinaldehído
/
Muerte Celular
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Ratas Sprague-Dawley
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Apoptosis
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Ganglión
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Microscopía Electrónica de Transmisión
/
Neuronas Retinianas
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Presión Intraocular
/
Isquemia
Límite:
Adult
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Humans
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Male
Idioma:
Ko
Revista:
Journal of the Korean Ophthalmological Society
Año:
1998
Tipo del documento:
Article