N omega-nitro-L-arginine-methyl ester inhibits electrocortical recovery subsequent to transient global brain ischemia in Mongolian gerbil.
Electrocorticographic (ECoG) activity remains isoelectric for about 15 min after transient (10 min) bilateral carotid arteries occlusion in mongolian gerbils. In this model of global forebrain ischemia N omega-Nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly delays the recovery of ECoG amplitude. Thus, the present experiments suggest that NO is involved in the cerebrovascular physiological response to brain ischemia.
Sancesario
G
G
Department of Public Health and Molecular Biology, University of Rome Tor Vergata, Italy.
Iannone
M
M
D'Angelo
V
V
Nisticò
G
G
Bernardi
G
G
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D001921:Brain / Q000378:metabolism / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D004569:Electroencephalography / Q000187:drug effects*; D005849:Gerbillinae / Q000502:physiology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000378:metabolism*
D009569:Nitric Oxide; D001120:Arginine; D019331:NG-Nitroarginine Methyl Ester