|
KMID : 0390119960360010225
|
|
Journal of Pusan Medical College
1996 Volume.36 No. 1 p.225 ~ p.236
|
|
|
Protective Effects of Inhibitors of Inducible Nitric Oxide Synthase on Focal Cerebral Ischemia of Rats
|
|
|
|
|
Abstract
|
|
|
Nitric oxide (NO) exerts both beneficial and detrimental effects in stroke. The beneficial effects are likely dependent upon endothelium-derived relaxing factor activity, whereas the injurious effects are probably via direct cytotoxicity. In the
present
study, it was aimed to investigate the involvement of NO in permanent focal cerebral ischemia by determining the effects of inhibitors of inducible NO synthase (iNOS) on cerebral ischemic damage and nitrite production in ischemic brain tissues.
Sprague-Dawley rate were subjected to right middle cerebral artery (MCA) occlusion using intraluminal thread technique.
1. Morphometrically detectable infarct was developed in the cortex and striatum identical to the territory of MCA starting 6 hours after MCA occlusion.
2. The size of infarct was significantly reduced by aminoguanidine (1or 10 mg/kg) and glibenclamide (0.1 or 1 mg/kg), respectively. However, the protective action was reversed by higher doses of aminoguanidine (100 mg/kg) and glibenclamide (10
mg/kg).
3. Dexamethasone (3 mg/kg) caused a marginal reduction in total infarct area in spite of no significant changes in infarct area of coronal slices.
4. Nw -nitro-L-arginine (1 mg/kg) was without effect on infarct size.
5. Brain nitrite production in the ischemic group was significantly higher than that in control group. The increase in nitrite production was significantly attenuated by iNOS inhibitors.
Based on these results, it is concluded that iNOS is largely expressed following facal cerebral ischemia and NO synthesis iNOS contributes to the ischemic brain damage. Thus, iNOS inhibition might be useful for the treatment of ischemic stroke.
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|