The effects of nitric oxide synthase inhibitor, L-NAME on no production during focal cerebral ischemia in rats: Could L-NAME be the future treatment of sudden deafness?


Balkan E., Balkan S., Ozben T., Serteser M. , Gumuslu S., Oguz N.

INTERNATIONAL JOURNAL OF NEUROSCIENCE, cilt.89, ss.61-77, 1997 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 89
  • Basım Tarihi: 1997
  • Doi Numarası: 10.3109/00207459708988465
  • Dergi Adı: INTERNATIONAL JOURNAL OF NEUROSCIENCE
  • Sayfa Sayısı: ss.61-77

Özet

Recent evidence in primary neuronal cell culture implicates NO as a mediator of glutamatergic neurotoxicity acting via N-methyl-D-aspartate (NMDA) receptors. In this study, we investigated the effects of inhibition of NOsynthase activity in focal cerebral ischemia in rats. Focal cerebral ischemia was produced by permanent occlusion of right MCA in urethane anesthetized rats. A number of indicators of brain NO production, nitrite and cGMP were determined in ipsilateral and contralateral cerebral cortex and cerebellum after 0, 10 and 60 minutes of focal cerebral ischemia. The same parameters were measured in rats pre- and posttreated with the potent Nitric oxide synthase (NOS) inhibitor, NW-nitro-L-arginine methyl ester (L-NAME).