Modulation of evoked cerebral blood flow under excessive blood supply and hyperoxic conditions

Citation
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
Citations number
31
Categorie Soggetti
Physiology
Journal title
JAPANESE JOURNAL OF PHYSIOLOGY
ISSN journal
0021521X → ACNP
Volume
50
Issue
1
Year of publication
2000
Pages
115 - 123
Database
ISI
SICI code
0021-521X(200002)50:1<115:MOECBF>2.0.ZU;2-X
Abstract
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.