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Nitric oxide and cerebral blood flow responses to hyperbaric oxygen
Ist Teil von
Journal of applied physiology (1985), 2000-04, Vol.88 (4), p.1381-1389
Ort / Verlag
United States: Am Physiological Soc
Erscheinungsjahr
2000
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
1 Institute of Evolutionary Physiology and
Biochemistry, Russian Academy of Sciences, St. Petersburg 199034, Russia; and 2 The F. G. Hall Laboratory, Duke
University Medical Center, Durham, North Carolina 27710
We
have tested the hypothesis that cerebral nitric oxide (NO) production
is involved in hyperbaric O 2 (HBO 2 )
neurotoxicity. Regional cerebral blood flow (rCBF) and
electroencephalogram (EEG) were measured in anesthetized rats during
O 2 exposure to 1, 3, 4, and 5 ATA with or without
administration of the NO synthase inhibitor
( N -nitro- L -arginine methyl
ester), L -arginine, NO donors, or the N -methyl- D -aspartate receptor inhibitor MK-801.
After 30 min of O 2 exposure at 3 and 4 ATA, rCBF decreased
by 26-39% and by 37-43%, respectively, and was sustained
for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia
nigra by one-third but, thereafter, gradually returned to preexposure
levels, preceding the onset of EEG spiking activity. Rats pretreated
with N -nitro- L -arginine methyl
ester and exposed to HBO 2 at 5 ATA maintained a low rCBF.
MK-801 did not alter the cerebrovascular responses to HBO 2
at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in
control rats but were ineffective during HBO 2 exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO 2 , but, as exposure time is
prolonged, NO production increases and augments rCBF in anticipation of
neuronal excitation.
oxygen toxicity; glutamate neurotransmission; central nervous
system