Nitric oxide is involved in sustained and delayed cell death of rat retina following transient ischemia

Nitric oxide is involved in sustained and delayed cell death of rat retina following transient... We have investigated the role of nitric oxide (NO) in the rat retina following ischemic injury induced by transient increase of intraocular pressure. The thickness of both the inner plexiform layer and inner nuclear layer decreased during early postischemic stages (up to 1 week). In late postischemic stages (2–4 weeks), the thickness of the outer nuclear layer (ONL) decreased markedly. Thus, mechanisms other than excitotoxic ones may contribute to postischemic retinal cell death. Treatment of rats with N G -nitro- l -arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, significantly reduced ischemic damage. Our findings suggest that NO is involved in the mechanism of ischemic injury, and plays a key role in the delayed and sustained cell death in the ONL following transient retinal ischemia. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Nitric oxide is involved in sustained and delayed cell death of rat retina following transient ischemia

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Publisher
Elsevier
Copyright
Copyright © 2000 Elsevier Science B.V.
ISSN
0006-8993
D.O.I.
10.1016/S0006-8993(00)02816-X
Publisher site
See Article on Publisher Site

Abstract

We have investigated the role of nitric oxide (NO) in the rat retina following ischemic injury induced by transient increase of intraocular pressure. The thickness of both the inner plexiform layer and inner nuclear layer decreased during early postischemic stages (up to 1 week). In late postischemic stages (2–4 weeks), the thickness of the outer nuclear layer (ONL) decreased markedly. Thus, mechanisms other than excitotoxic ones may contribute to postischemic retinal cell death. Treatment of rats with N G -nitro- l -arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, significantly reduced ischemic damage. Our findings suggest that NO is involved in the mechanism of ischemic injury, and plays a key role in the delayed and sustained cell death in the ONL following transient retinal ischemia.

Journal

Brain ResearchElsevier

Published: Oct 27, 2000

References

  • Diversity of glutamate receptors in the mammalian retina
    Brandstätter, J.H.; Koulen, P.; Wässle, H.
  • Ischemia-induced neuronal apoptosis
    Choi, D.W.
  • Nitric oxide: a review of its role in retinal function and disease
    Goldstein, I.M.; Ostwald, P.; Roth, S.
  • A comparison of the effects of l -NAME, 7-NI and L-NIL on carrageenan-induced hindpaw oedema and NOS activity
    Handy, R.L.; Moore, P.K.

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