title: Characterization of suppression of nitric oxide production by carbon monoxide poisoning in the striatum of free-moving rats, as determined by in vivo brain microdialysis.
abstract: We examined the effect of carbon monoxide (CO) poisoning on the nitric oxide (NO) system in the striatum of free-moving rats by means of in vivo brain microdialysis. The extracellular levels of the oxidative NO products, nitrite (NO(2)(-)) and nitrate (NO(3)(-)), decreased during exposure to CO at 3000 ppm for 40 min, a condition which causes CO poisoning. The extracellular levels of citrulline (Cit; a by-product of NO production) and arginine (Arg; an NO precursor) also decreased during CO exposure. Following reoxygenation by withdrawal of CO, the NO(2)(-) and NO(3)(-) levels gradually recovered to the control values, though Arg and Cit remained at lower levels, except for a rapid, but transient, recovery shortly before and after reoxygenation, respectively. Simultaneous application of exogenous L-Arg (50 and 100 mM) with CO exposure attenuated the decreases in NO(2)(-) and NO(3)(-) during the CO exposure and accelerated their recovery following reoxygenation. However, D-Arg (100 mM) had no effect on the decrease in NO(2)(-) and NO(3)(-), except for slight and transient attenuation shortly after reoxygenation. Exogenous L-Cit (10 and 100 mM) failed to attenuate the CO-induced decrease in NO(2)(-) and NO(3)(-) levels. The decrease in the NO(2)(-) and NO(3)(-) levels during 8% O(2) exposure for 40 min, which was comparable with that in response to 3000 ppm CO, was resistant to exogenous 100 mM L-Arg, but the recovery of the NO(2)(-) and NO(3)(-) levels following reoxygenation was strongly accelerated. These findings suggest that CO poisoning suppresses NO production in rat striatum in vivo though a mechanism which may not be common with that in hypoxic hypoxia.
authors.affiliation: Department of Forensic Medicine, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, 160-8402, Tokyo, Japan. s-hara@tokyo-med.ac.jp
authors.forename: Shuichi
authors.initials: S
authors.lastname: Hara
authors.forename: Toshiji
authors.initials: T
authors.lastname: Mukai
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Kurosaki
authors.forename: Fumi
authors.initials: F
authors.lastname: Kuriiwa
authors.forename: Takahiko
authors.initials: T
authors.lastname: Endo
mesh_terms: D000818:Animals; D001120:Arginine / Q000032:analysis / Q000378:metabolism; D002249:Carbon Monoxide Poisoning / Q000378:metabolism*; D002956:Citrulline / Q000032:analysis; D003342:Corpus Striatum / Q000378:metabolism / Q000503:physiopathology*; D005110:Extracellular Space / Q000737:chemistry; D007536:Isomerism; D008297:Male; D017551:Microdialysis; D009068:Movement; D009566:Nitrates / Q000032:analysis; D009569:Nitric Oxide / Q000096:biosynthesis*; D009573:Nitrites / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D009566:Nitrates; D009573:Nitrites; D002956:Citrulline; D009569:Nitric Oxide; D001120:Arginine