Abstract
The recent advances in the histopathology of ischemia have set forth new proposals,
particularly in regard to excitotoxicity by the glutamate receptor, NMDA. The participation
of the nitric oxide (NO) in normal and pathological conditions and its relationship
with toxicity in ischemia, suggest new alternatives for the modulation of the NMDA
receptor REDOX site through its pharmacologic manipulation. This event would potentially
limit the consequences of the activationcalcium flow and the production of peroxoinitrite
during the ischemic phenomenon. The present work delivers two proposals: 1) A modified
technique to the ones that have been described, of endovascular, without craniectomy,
for experimental cerebral ischemia in Wistar rats, and with particular harmful effect
upon the hippocampus. 2) It promotes the use of nitrates as an additional alternative
to other elements, in order to restrict excitotoxicity in the described experimental
cerebral ischemia, and paying attention to CA1 - CA2 of the hippocampus. This area,
specially sensitive to hypoxia-ischemia, offers an excellent study option for focal,
experimental, cerebral ischemia associated with toxicity mediated by excitatory amino
acids, since it stores an important concentration of NMDA receptors (R1/R2 A) as well
as endothelial nitric oxide synthase. Our parameters are supported by quantitative-qualitative
cell analysis, and not by the extension of the stroke which offers a more objective
perspective upon the assessment of the focal ischemic event. By means of this technique,
these results confirm the extent of the ischemic injuryto the cell at the level of
the hippocampus compared to a control/basal group, p = 0.0006. Furthermore, it suggests
a neuroprotective effect of isosorbide dinitrate since it preserves the viable cells,
and limits the appearance of hypoxic-ischemic cells at the hippocampus when the middle
cerebral artery (MCA) is occluded endovascularly, as compared to the animals with
no treatment P = 0.0080. However, other research lines are needed to compare the efficacy
of this present work with other therapeutic proposals.
Key words
Focal ischemia - Neuroprotection - N-Methyl-D-aspartate (NMDA) - Nitric oxide
