Does hypercapnia-induced cerebral vasodilation modulate the hemodynamic response to neural activation?

Increases in cerebral blood flow produced by vasoactive agents will increas e blood oxygen level-dependent (BOLD) MRI signal intensity. The effects of such vasodilation on activation-related signal changes are incompletely cha racterized. The two signal changes may be simply additive or there may be m ore a complex interaction. To investigate this, BOLD MRI was performed in f our normal male subjects using T2*-weighted echo planar imaging; brain volu mes were acquired every 6.2 s, using a Siemens VISION scanner operating at 2 Tesla; each volume consisted of 64 sequential transverse slices (64 x 64 pixels per slice, 3 x 3 x 3 mm). Sixteen periods of visual stimulation were produced using a flickering checkerboard (8 Hz, 31 s On/31 s Off); this wa s coupled with five periods of hypercapnia (4% inspired CO2, 62 s On/124 s Off). Data were analyzed using SPM96, Mean signal intensity, calculated glo bally for the whole brain, closely mirrored changes in the partial pressure of end-tidal CO2 (PCO2), and hypercapnia was associated with widespread si gnificant signal increases (P < 0.001), predominantly within grey matter. A s expected, the visual stimulation produced significant signal changes with in the occipital cortex (P < 0.001), Within the occipital cortex, no signif icant interactions (P > 0.001) between the effects of the visual stimulatio n and PCO2 were present. The increases in PCO2 imposed dynamically in the p resent study would increase cerebral blood flow by between 25 and 40%, an i ncrease within the physiological range and comparable to that induced by ne ural activation. With this flow change the effects of vasodilation, on an a ctivation-related signal change, are simply additive. (C) 2001 Academic Pre ss.