Adachi K, Fujita Y, Morizane C, Akaike A, Ueda M, Satoh M, Masai H, Kashii S, Honda Y
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Japan.
Eur J Pharmacol. 1998 May 29;350(1):53-7. doi: 10.1016/s0014-2999(98)00317-3.
This study was performed to examine the roles of body temperature, NMDA receptors and nitric oxide (NO) synthase in post-ischemic retinal injury in rats. Cell loss in the ganglion cell layer and thinning of the inner plexiform layer were observed 7 days after ischemia. Cell loss in the ganglion cell layer but not thinning of the inner plexiform layer was reduced by hypothermia during ischemia. Intravenous injection of dizocilpine (MK-801) or Nomega-nitro-L-arginine methyl ester (L-NAME) prior to ischemia ameliorated retinal injury. These results suggest that activation of NO synthase following NMDA receptor stimulation is involved in ischemia-induced retinal injury.
