The blood oxygenation level‐dependent (BOLD) effect in functional magnetic resonance imaging depends on at least partial uncoupling between cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) changes. By measuring CBF and BOLD simultaneously, the relative change in CMRO2 can be estimated during neural activity using a reference condition obtained with known CMRO2 change. In this work, nine subjects were studied at a magnetic field of 1.5 T; each subject underwent inhalation of a 5% carbon dioxide gas mixture as a reference and two visual stimulation studies. Relative CBF and BOLD signal changes were measured simultaneously using the flow‐sensitive alternating inversion recovery (FAIR) technique. During hypercapnia established by an end‐tidal CO2 increase of 1.46 kPa, CBF in the visual cortex increased by 47.3 ± 17.3% (mean ± SD; n = 9), and ΔR*2 was −0.478 ± 0.147 sec−1, which corresponds to BOLD signal change of 2.4 ± 0.7% with a gradient echo time of 50 msec. During black/white visual stimulation reversing at 8 Hz, regional CBF increase in the visual cortex was 43.6 ± 9.4% (n = 18), and ΔR*2 was −0.114 ± 0.086 sec−1, corresponding to a BOLD signal change of 0.6 ± 0.4%. Assuming that CMRO2 does not change during hypercapnia and that hemodynamic responses during hypercapnia and neural stimulation are similar, relative CMRO2 change was determined using BOLD biophysical models. The average CMRO2 change in the visual cortex ranged from 15.6 ± 8.1% (n = 18) with significant cerebral blood volume (CBV) contribution to 29.6 ± 18.8% without significant CBV contribution. A weak positive correlation between CBF and CMRO2 changes was observed, suggesting the CMRO2 increase is proportional to the CBF increase. Magn Reson Med 41:1152–1161, 1999. © 1999 Wiley‐Liss, Inc.
Local increases in neuronal activity within the brain lead to dilation of blood vessels and to increased regional cerebral blood flow. Increases in extracellular potassium concentration are known to dilate cerebral arterioles. Recent studies have suggested that the potassium released by active neurons is transported through astrocytic glial cells and released from their endfeet onto blood vessels. The results of computer simulations of potassium dynamics in the brain indicate that the release of potassium from astrocyte endfeet raises perivascular potassium concentration much more rapidly and to higher levels than does diffusion of potassium through extracellular space, particularly when the site of a potassium increase is some distance from the vessel wall. On the basis of this finding, it is proposed that the release of potassium from astrocyte endfeet plays an important role in regulating regional cerebral blood flow in response to changes in neuronal activity.Roy and Sherrington, in 1890, suggested that "the brain possesses an intrinsic mechanism by which its vascular supply can be varied locally in correspondence with local variations of functional activity" (1, p. 105). Such an intrinsic homeostatic mechanism would help to maintain an adequate supply of oxygen and nutrients to the brain despite widely varying levels of neuronal activity. Although the existence of such a regulatory process has been established (2-5), the mechanism that links neuronal activity and regional cerebral blood flow (rCBF) remains unknown. Interstitial concentrations of potassium and hydrogen ions, adenosine, and several neuro-transmitters vary with neuronal activity. These substances all cause changes in arteriole diameter (6,7) and have been implicated in the regulation of rCBF. However, the relative importance of each of these factors is not known.varies widely during periods of neuronal activity and can rise from a quiescent level of approximately 3 mM to a maximum level of more than 10 mM (8). Cerebral arteries and arterioles (but not capillaries) are extremely sensitive to changes in K + concentration, increasing in diameter as much as 50% in response to a change in [K + ] o from 3 to 10 mM (9,10). This sensitivity to K + could be an important factor in regulating rCBF. Potassium released by active neurons could diffuse through extracellular space to the ablumenal wall of arterioles and cause arteriole dilation. The resulting decrease in vascular resistance (11) would increase rCBF, thus bringing a greater supply of oxygen to precisely the region where it is needed, to the activated portion of the brain. However, arterioles are widely spaced within the brain [they are often separated by more than 500 μim (12)] and may not necessarily be near regions of activated tissue. Thus, the K + released by active neurons would have to diffuse tens or hundreds of micrometers before reaching arterioles and effecting dilation.
Specific cerebral lesions have shown the crucial role of the brain in the control of micturition. The precise identification of the anatomical cerebral structures involved in micturition can contribute to a better understanding of the control of micturition and the development of therapeutic models. Various neuropathological and animal studies have referred to the medulla oblongata, pons, limbic system, superior frontal lobe and premotor cortical regions as areas implicated in micturition control. The aim of this study was to investigate whether the activity of these areas during micturition can be confirmed by PET in normal men. The distribution of the regional cerebral blood flow after bolus injection of (15)O water was used as an indirect measure of cerebral activation. PET scans were performed during the following three conditions: (i) at rest with the bladder empty; (ii) during simulated micturition after instillation of isotonic saline into the urinary bladder; and (iii) the withholding of urine (saline). Normal micturition using this model was achieved in eight out of 12 right-handed normal subjects. The changes in bladder contraction, bladder pressure and intra-abdominal pressure were monitored on-line during the whole scanning session by a cystometry device. The images were analysed using statistical parametric mapping at a significance threshold of P < 0.05 with correction for multiple independent comparisons. Micturition versus rest was associated with bilateral activation of areas close to the postcentral gyrus, inferior frontal gyrus, globus pallidus, cortex cerebelli, vermis and midbrain. On the left side, activation of the middle frontal gyrus, superior frontal gyrus, superior precentral gyrus, thalamus and the caudal part of the anterior cingulate gyrus was seen, while on the right side we found activation in the supramarginal gyrus, mesencephalon and insula. When the threshold value was lowered to P < 0.001 (Z > 3.09) without correction for multiple comparisons, we found additional activation in the medial pontine tegmentum, mesencephalon, right thalamus, right middle frontal gyrus and left insula. When urine- withholding was compared with rest, the left insula showed a tendency to activate. We conclude from this study, in which urinary bladder contraction was verified cystometrically, that the onset and maintenance of micturition in normal men is associated with a vast network of cortical and subcortical regions, confirming observations from clinical and animal studies.
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