title: Blood flow and ionic responses in the awake brain due to carbon monoxide.
abstract: This study examined the effect of 2000 ppm CO on the brain of an awake rat. Measurements of regional perfusion as well as metabolic, ionic and electrical activities were used to examine whether mechanisms responsible for changes in brain perfusion were separable from those attributable to compromises in neuronal metabolism. Exposure to 2000 ppm CO resulted in elevation of cerebral blood flow. The stability of mitochondrial NADH redox level during CO exposure indicated that tissue hypoxia did not develop. The elevation in blood flow was inhibited by L-nitroarginine methyl ester, indicating that nitric oxide was responsible for the CO-induced elevation in blood flow. Exposure to 2000 ppm CO also triggered a significant decrease in pH and rise in extracellular potassium ion, possibly due to ion-pump inhibition. The amplitude of the electrocorticogram wave activity decreased, indicative of a compromise to physiological activity. These changes were not observed in rats anesthetized with pentobarbital during CO exposure, although anesthesia had no effect on the CO-induced elevation in blood flow and there was still no change in mitochondrial NADH redox level. We concluded that CO acts by separate mechanisms to alter cerebral vasoactivity and neuronal metabolic responses and that both processes are independent of hypoxic stress.
authors.affiliation: Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel.
authors.forename: Avivit
authors.initials: A
authors.lastname: Mendelman
authors.forename: Nili
authors.initials: N
authors.lastname: Zarchin
authors.forename: Sigal
authors.initials: S
authors.lastname: Meilin
authors.forename: Esther
authors.initials: E
authors.lastname: Guggenheimer-Furman
authors.forename: S R
authors.initials: SR
authors.lastname: Thom
authors.forename: Avraham
authors.initials: A
authors.lastname: Mayevsky
mesh_terms: D000777:Anesthetics / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000503:physiopathology; D002248:Carbon Monoxide / Q000633:toxicity*; D002249:Carbon Monoxide Poisoning / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D004569:Electroencephalography / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects* / Q000502:physiology; D002534:Hypoxia, Brain / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D007477:Ions / Q000378:metabolism*; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009243:NAD / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015996:Survival Rate; D014851:Wakefulness / Q000187:drug effects / Q000502:physiology
chemical_list: D000777:Anesthetics; D007477:Ions; D009243:NAD; D009569:Nitric Oxide; D002248:Carbon Monoxide; D019001:Nitric Oxide Synthase; D011188:Potassium