Abstract
The predictive value of increase in cerebral blood flow (CBF) was examined to detect hyperbaric oxygen (HBO2)-induced electrical discharge in artificially ventilated rats at three PaCO2 levels under 5 atmospheric pressures. The possible involvement of NO production in the mechanism of the increase in CBF was also assessed by measurement of major NO metabolites (NO2 - plus NO3 -) using a microdialysis technique at the left parietal cortex during HBO2 exposure. The onset times of electrical discharge, measured in the right frontal region, were significantly prolonged and shortened in the low PaCO2 group (79±21 min) and high PaCO2 group (27±7 min), respectively, compared to that in the normal PaCO2 group (37±5 min). Increase in CBF (200% of the pre-exposure level) was observed in every animal and was sustained until the appearance of electrical discharge. The onset time of increase in CBF was closely related to that of electrical discharge (R2=0.987), and the durations of increase in CBF were almost identical (11-14 min in mean) regardless of the PaCO2 level. The level of NO2 - plus NO3 - was unaffected by the initiation of HBO2 exposure and simultaneously increased up to 246±59% of control level with the onset of increase in CBF. There was a close relationship between changes in CBF and levels of NO2 - plus NO3 - (R2=0.544). These results indicate that monitoring of CBF is useful for the prediction of electrical discharge in artificially ventilated rats regardless of their PaCO2 levels and that the increase in NO production is related to the mechanism of increase in CBF.
| Original language | English |
|---|---|
| Pages (from-to) | 131-140 |
| Number of pages | 10 |
| Journal | Brain Research |
| Volume | 918 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Nov 9 2001 |
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Keywords
- Cerebrovascular circulation
- Electroencephalography
- Hyperbaric oxygenation
- Microdialysis
- Nitric oxide
- Seizure
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Changes in nitric oxide production and cerebral blood flow before development of hyperbaric oxygen-induced seizures in rats. / Sato, Tetsufumi; Takeda, Yoshimasa; Hagioka, Shingo; Zhang, Shan; Hirakawa, Masahisa.
In: Brain Research, Vol. 918, No. 1-2, 09.11.2001, p. 131-140.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Changes in nitric oxide production and cerebral blood flow before development of hyperbaric oxygen-induced seizures in rats
AU - Sato, Tetsufumi
AU - Takeda, Yoshimasa
AU - Hagioka, Shingo
AU - Zhang, Shan
AU - Hirakawa, Masahisa
PY - 2001/11/9
Y1 - 2001/11/9
N2 - The predictive value of increase in cerebral blood flow (CBF) was examined to detect hyperbaric oxygen (HBO2)-induced electrical discharge in artificially ventilated rats at three PaCO2 levels under 5 atmospheric pressures. The possible involvement of NO production in the mechanism of the increase in CBF was also assessed by measurement of major NO metabolites (NO2 - plus NO3 -) using a microdialysis technique at the left parietal cortex during HBO2 exposure. The onset times of electrical discharge, measured in the right frontal region, were significantly prolonged and shortened in the low PaCO2 group (79±21 min) and high PaCO2 group (27±7 min), respectively, compared to that in the normal PaCO2 group (37±5 min). Increase in CBF (200% of the pre-exposure level) was observed in every animal and was sustained until the appearance of electrical discharge. The onset time of increase in CBF was closely related to that of electrical discharge (R2=0.987), and the durations of increase in CBF were almost identical (11-14 min in mean) regardless of the PaCO2 level. The level of NO2 - plus NO3 - was unaffected by the initiation of HBO2 exposure and simultaneously increased up to 246±59% of control level with the onset of increase in CBF. There was a close relationship between changes in CBF and levels of NO2 - plus NO3 - (R2=0.544). These results indicate that monitoring of CBF is useful for the prediction of electrical discharge in artificially ventilated rats regardless of their PaCO2 levels and that the increase in NO production is related to the mechanism of increase in CBF.
AB - The predictive value of increase in cerebral blood flow (CBF) was examined to detect hyperbaric oxygen (HBO2)-induced electrical discharge in artificially ventilated rats at three PaCO2 levels under 5 atmospheric pressures. The possible involvement of NO production in the mechanism of the increase in CBF was also assessed by measurement of major NO metabolites (NO2 - plus NO3 -) using a microdialysis technique at the left parietal cortex during HBO2 exposure. The onset times of electrical discharge, measured in the right frontal region, were significantly prolonged and shortened in the low PaCO2 group (79±21 min) and high PaCO2 group (27±7 min), respectively, compared to that in the normal PaCO2 group (37±5 min). Increase in CBF (200% of the pre-exposure level) was observed in every animal and was sustained until the appearance of electrical discharge. The onset time of increase in CBF was closely related to that of electrical discharge (R2=0.987), and the durations of increase in CBF were almost identical (11-14 min in mean) regardless of the PaCO2 level. The level of NO2 - plus NO3 - was unaffected by the initiation of HBO2 exposure and simultaneously increased up to 246±59% of control level with the onset of increase in CBF. There was a close relationship between changes in CBF and levels of NO2 - plus NO3 - (R2=0.544). These results indicate that monitoring of CBF is useful for the prediction of electrical discharge in artificially ventilated rats regardless of their PaCO2 levels and that the increase in NO production is related to the mechanism of increase in CBF.
KW - Cerebrovascular circulation
KW - Electroencephalography
KW - Hyperbaric oxygenation
KW - Microdialysis
KW - Nitric oxide
KW - Seizure
UR - http://www.scopus.com/inward/record.url?scp=0035834331&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035834331&partnerID=8YFLogxK
U2 - 10.1016/S0006-8993(01)02984-5
DO - 10.1016/S0006-8993(01)02984-5
M3 - Article
C2 - 11684051
AN - SCOPUS:0035834331
VL - 918
SP - 131
EP - 140
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 1-2
ER -