Effects of carbon monoxide on the brain may be mediated by nitric
oxide .
Meilin, S., G. G. Rogatsky, S. R. Thom, N. Zarchin, E. Guggenheimer
-Furman, and A. Mayevsky.
Department of Life Sciences, Bar-Ilan University, Ramat-Gan 52900,
Israel and Institute for Environmental Medicine, University of
Pennsylvania Medical Center, Philadelphia, PA., U.S.A.
APStracts 3:0216A, 1996.
Carbon monoxide (CO) is known to be a toxic molecule due to the high
affinity of hemoglobin for it. However, it has recently been shown
that low doses of CO may play a physiological role. The aim of the
present study was to examine processes occurring in the brain during
exposure to 1000 ppm CO which result in an increase in cerebral blood
flow (CBF) but are not accompanied by changes in oxidative
metabolism. This study was carried out in awake rats using the
multiprobe assembly (MPA) developed in this laboratory for the
simultaneous, continuous measurement of CBF, intramitochondrial NADH
redox levels, DC potential, extracellular concentration of K+, Ca2+
and H+ as well as the electrocorticogram. Exposure to 1000 ppm CO in
air resulted in increased CBF without any concomitant changes in any
of the other metabolic or ionic parameters measured. This indicates
that tissue hypoxia was not the trigger for this vasodilation.
Injection of Nitro-Arginine (N-Arg), an NO Synthase (NOS) inhibitor,
prior to exposure to CO effectively blocked the increase in CBF which
was observed when the animal was exposed to CO without prior
injection of N-Arg. Furthermore, Electrocorticogram (ECoG) depression
was observed following the combined treatment of N-Arg and CO. In
conclusion, exposure to relatively low doses of CO apparently does
not have a deleterious effect on oxidative metabolism, since the
increase in CBF following this exposure is sufficient to prevent
changes in oxidative metabolism as indicated by the fact that NADH
levels remained constant. This protective autoregulatory effect may
be mediated by NO.
Received 26 June 1995; accepted in final form 10 April 1996.
APS Manuscript Number A690-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96