T. Matsuura et al., Modulation of evoked cerebral blood flow under excessive blood supply and hyperoxic conditions, JPN J PHYSL, 50(1), 2000, pp. 115-123
We measured the field potential and local cerebral blood flow (LCBF) using
laser-Doppler flowmetry in alpha-chloralose anesthetized rats during activa
tion of the somatosensory cortex by electrical stimulation of the hind paw
under independent administration of additional carbon dioxide and oxygen. T
he aim of this study was to test the hypothesis that the increase in LCBF d
uring activation of the cortex (evoked LCBF) is not directed toward supplyi
ng oxygen for oxidative metabolism. Under the hypercapnic condition (Pa-CO2
= 74.9+/-14.3 mmHg), the baseline LCBF was about 46.5% higher than that un
der the normocapnic condition (Pa-CO2 = 35.7+/- 2.1 mmHg) (p < 0.001), but
after normalization for each baseline (divided by the prestimulus level), t
here was no significant difference in the peak value and the rise time of n
ormalized evoked LCBF. On the other hand, the baseline level of LCBF under
the hyperoxic condition (Pa-O2 = 479.4+/-77.2 mmHg) was about 5.0% lower th
an that under the normoxic condition (Pa-O2 = 105.5+/-7.8 mmHg) (p < 0.01),
suggesting mild vasoconstriction under the condition of hyperoxia at rest.
The peak value of normalized evoked LCBF under the hyperoxic condition was
about 6.5% higher than that under the normoxic condition (p < 0.05). In ad
dition, the rise time of evoked LCBF was earlier under the hyperoxic condit
ion (0.37+/-0.16 s) than that under the normoxic condition (0.52+/-0.12 s)
(p < 0.01). The field potential measured during stimulation under hypercapn
ic and hyperoxic conditions was not significantly different when compared w
ith that under normal gas conditions. These results support our hypothesis
and suggest that the excess oxygen is involved in the mechanism underlying
the regulation of LCBF.