Hemodynamics of local cerebral blood flow induced by somatosensory stimulation under normoxia and hyperoxia in rats. |
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Authors: | T Matsuura K Kashikura I Kanno |
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Affiliation: | Akita Laboratory, Japan Science and Technology Corporation, Akita Research Institute of Brain and Blood Vessels, 6-10 Senshu-kubota machi, Akita 010-0874, Japan. matsuura@akita-noken.go.jp |
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Abstract: | We observed changes in the local cerebral blood flow (LCBF), red blood cell (RBC) concentration and RBC velocity in alpha-chloralose anesthetized rats using laser-Doppler flowmetry during activation of the somatosensory cortex following electrical stimulation of the hind paw under hyperoxia (PaO(2)=513.5+/-48.4 mmHg; mean+/-S.D.) and normoxia (PaO(2)=106.4+/-8.4 mmHg). Electrical stimuli of 5 and 10 Hz (pulse width 0.1 ms) with an intensity of 1.5 mA were applied for 5 s (n=13 at 5 Hz, n=9 at 10 Hz). Baseline levels of LCBF and RBC concentration under hyperoxia were, respectively, 5.6+/-3.3 and 8.8+/-3.0% lower than those under normoxia (P<0.05), and that of RBC velocity under hyperoxia was slightly higher than that under normoxia (NS), suggesting mild vasoconstriction at rest under hyperoxia. At 5 Hz stimulation, after normalization to each baseline level, normalized response magnitudes of LCBF, RBC concentration and RBC velocity under hyperoxia were, respectively, 68.2+/-48.0, 71.1+/-65.5 and 66.0+/-56.3% greater than those under normoxia (P<0.05). At 10-Hz stimulation, normalized response magnitudes of LCBF and RBC concentration under hyperoxia were, respectively, 44.6+/-32.0 and 55.9+/-43.5% greater than those under normoxia (P<0.05), although a significant difference in the normalized response magnitude of RBC velocity was not detected between both conditions. The evoked LCBF under hyperoxia increased earlier, by approximately 0.15 s, than that under normoxia regardless of the stimulus frequency (P<0.05). These results suggest the involvement of oxygen interaction on the regulation of LCBF during neuronal activation. |
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