Effects of carbon monoxide on the brain may be mediated by nitric oxide

摘要: Carbon monoxide (CO) is known to be a toxic molecule due the high affinity of hemoglobin for it. However, it has recently been shown that low doses CO may play physiological role. The aim present study was examine processes occurring in brain during exposure 1,000 parts per million result an increase cerebral blood flow (CBF) but are not accompanied by changes oxidation metabolism. This carried out awake rats with multiprobe assembly developed this laboratory simultaneous continuous measurement CBF, intramitochondrial NADH redox levels, direct current potential, and extracellular concentrations K+, Ca2+, H+ as well electrocorticogram. Exposure air resulted increased CBF without any concomitant other metabolic or ionic parameters measured. indicates tissue hypoxia trigger vasodilation. Injection N omega-nitro-L-arginine (L-NNA), nitric oxide synthase inhibitor, before effectively blocked observed when animal exposed prior injection L-NNA. Furthermore, electrocorticographic depression after combined treatment L-NNA CO. In conclusion, relatively apparently does have deleterious effect on oxidative metabolism because sufficient prevent metabolism, indicated fact levels remained constant. protective autoregulatory mediated oxide.