Abstract
Nitric Oxide (NO) was discovered as cerebral neurotransmitter and it has been implicated as a mediator of neurotoxicity expeciaily in response to glutamate. NO is synthesized from L-arginine and after a 1 second half-life it is decomposed to nitrite and nitrate via reaction with Superoxide anion and intermediate production of peroxinitrites. In order to understand NO role in cerebral ischemia it is important to know at which concentration it is formed in vivo and his time course during and after ischemia. In our experimental model of photoinduced cerebral cortical ischemia in rats, perfusate was collected via microdialysis and nitrite and nitrate were determined by HPLC method during ischemia and in the 4 hours after ischemia. An elevation of total NO catabolites (nitrite + nitrate) was seen from induction of ischemia with a concentration peak at the second hour after ischemia. The time course of nitrate concentration increased from the induction with a peak at the first hour while nitrite concentration increased from the second hour. The difference observed in NO metabolic pathway supports the hypotesis of a critical role of this neurotransmitter in cerebral ischemia and sive a rational base to new therapeutic strategies.
| Original language | English |
|---|---|
| Pages (from-to) | 47 |
| Number of pages | 1 |
| Journal | Italian Journal of Neurological Sciences |
| Volume | 18 |
| Issue number | 4 |
| Publication status | Published - 1997 |
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology