| Research Abstract |
Nitric oxide (NO) serves as a mediator of glutamate neurotoxlclty in the brain and NO synthase (NOS) inhibitors retard the development of brain acidosis during permanent focal cerebral ischemia. These findings suggest that NOS inhibitors might ameliorate ischemic brain injury. On the other hand, NOS inhibitors are thought to - reduce CBF, probably due to dose-dependent vasoconstrictive action, and thus may enhance the : ischemic injury. So, in this study, to clarify whether NO is either neurotoxic or neuroprotective, we examined the change of MRI signal intensity (SI) of the focal ischemlc region in rats given various doses of an NOS Inhibitor, N G-monoethyl-L-arginine (NMMA).
Sprague-Dawley : 58 rats (anesthesia : halothauc) right middle cerebral artery (MCA) permanent occlusion transvascular approach : nylon 2/0 suture.
1. An increase of signal intensity of the T2 weighted image Indicates brain Infarction and/or edema due to lschemia.
2. The effect of NMMA on brain ischemia at 6 hours after MCA occlusion is non protective for the lscheniic side, but protective for the non-sichemic cortex (significant decrease of signal intensity).
3. The effect of NMMA on brain lschemla at 24 hours after MCA occlusion is protective for the ischemic cortex.
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