Blockade of nitric oxide formation by N omega-nitro-L-arginine mitigates ischemic brain edema and subsequent cerebral infarction in rats.
In order to investigate whether or not nitric oxide (NO) formation underlies the cellular mechanisms of ischemic brain damage, we examined the effects of N omega-nitro-L-arginine (L-NNA), a NO synthase inhibitor, on ischemic brain edema and subsequent infarction in rats with middle cerebral artery occlusion (MCAo). For this purpose, administrations of L-NNA (1 mg/kg, i.p.) to each animal were done at the time of 5 min, 3, 6 and 24 h after MCAo, respectively. It was shown from this study that L-NNA significantly mitigated ischemic cerebral edema, and histological examinations revealed that this compound markedly reduced infarction size that occurred following MCAo. These results strongly suggest that NO formation is at least partly involved in the pathogenetic mechanisms of ischemic brain edema and subsequent cerebral infarction.
Nagafuji
T
T
Department of Neurosurgery, Saitama Medical Center/School, Japan.
Matsui
T
T
Koide
T
T
Asano
T
T
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D001923:Brain Chemistry / Q000187:drug effects*; D001929:Brain Edema / Q000188:drug therapy*; D002545:Brain Ischemia / Q000188:drug therapy*; D002536:Cerebral Arteries / Q000502:physiology; D002544:Cerebral Infarction / Q000188:drug therapy*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D019335:Nitroarginine; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism
D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine; D012964:Sodium; D011188:Potassium