Arterial fraction of cerebral blood volume in humans measured by positron emission tomography

2001 ◽  
Vol 15 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Ito ◽  
Iwao Kanno ◽  
Hidehiro Iida ◽  
Jun Hatazawa ◽  
Eku Shimosegawa ◽  
...  
2001 ◽  
Vol 21 (12) ◽  
pp. 1472-1479 ◽  
Author(s):  
Hidehiko Okazawa ◽  
Hiroshi Yamauchi ◽  
Kanji Sugimoto ◽  
Hiroshi Toyoda ◽  
Yoshihiko Kishibe ◽  
...  

To evaluate changes in cerebral hemodynamics and metabolism induced by acetazolamide in healthy subjects, positron emission tomography studies for measurement of cerebral perfusion and oxygen consumption were performed. Sixteen healthy volunteers underwent positron emission tomography studies with15O-gas and water before and after intravenous administration of acetazolamide. Dynamic positron emission tomography data were acquired after bolus injection of H215O and bolus inhalation of15O2. Cerebral blood flow, metabolic rate of oxygen, and arterial-to-capillary blood volume images were calculated using the three-weighted integral method. The images of cerebral blood volume were calculated using the bolus inhalation technique of C15O. The scans for cerebral blood flow and volume and metabolic rate of oxygen after acetazolamide challenge were performed at 10, 20, and 30 minutes after drug injection. The parametric images obtained under the two conditions at baseline and after acetazolamide administration were compared. The global and regional values for cerebral blood flow and volume and arterial-to-capillary blood volume increased significantly after acetazolamide administration compared with the baseline condition, whereas no difference in metabolic rate of oxygen was observed. Acetazolamide-induced increases in both blood flow and volume in the normal brain occurred as a vasodilatory reaction of functioning vessels. The increase in arterial-to-capillary blood volume made the major contribution to the cerebral blood volume increase, indicating that the raise in cerebral blood flow during the acetazolamide challenge is closely related to arterial-to-capillary vasomotor responsiveness.


1984 ◽  
Vol 4 (3) ◽  
pp. 317-322 ◽  
Author(s):  
Adriaan A. Lammertsma ◽  
David J. Brooks ◽  
Ronald P. Beaney ◽  
David R. Turton ◽  
Malcolm J. Kensett ◽  
...  

A method is described for measuring the regional cerebral-to-large vessel haematocrit ratio using inhalation of carbon-11-labelled carbon monoxide and the intravenous injection of carbon-11-labelled methyl-albumin in combination with positron emission tomography. The mean value in a series of nine subjects was 0.69. This is ∼20% lower than the value of 0.85 previously reported. It is concluded that previous measurements of regional cerebral blood volume using a haematocrit ratio of 0.85 will have underestimated the value of regional cerebral blood volume by 20%.


2010 ◽  
Vol 65 (3) ◽  
pp. 744-749 ◽  
Author(s):  
Jinsoo Uh ◽  
Ai-Ling Lin ◽  
Kihak Lee ◽  
Peiying Liu ◽  
Peter Fox ◽  
...  

2005 ◽  
Vol 25 (7) ◽  
pp. 852-857 ◽  
Author(s):  
Hiroshi Ito ◽  
Masanobu Ibaraki ◽  
Iwao Kanno ◽  
Hiroshi Fukuda ◽  
Shuichi Miura

Hypercapnia induces cerebral vasodilation and increases cerebral blood volume (CBV), and hypocapnia induces cerebral vasoconstriction and decreases CBV. Cerebral blood volume measured by positron emission tomography (PET) is the sum of three components, that is, arterial, capillary, and venous blood volumes. Changes in arterial blood volume ( Va) and CBV during hypercapnia and hypocapnia were investigated in humans using PET with H215O and 11CO. Arterial blood volume was determined from H215O PET data by means of a two-compartment model that takes Va into account. Baseline CBV and values during hypercapnia and hypocapnia in the cerebral cortex were 0.034 ± 0.003, 0.038 ± 0.003, and 0.031 ± 0.003 mL/mL (mean ± s.d.), respectively. Baseline Va and values during hypercapnia and hypocapnia were 0.015 ± 0.003, 0.025 ± 0.011, and 0.007 ± 0.003 mL/mL, respectively. Cerebral blood volume changed significantly owing to changes in PaCO2, and Va changed significantly in the direction of CBV changes. However, no significant change was observed in venous plus capillary blood volume (= CBV- Va). This indicates that changes in CBV during hypercapnia and hypocapnia are caused by changes in arterial blood volume without changes in venous and capillary blood volume.


2001 ◽  
Vol 21 (5) ◽  
pp. 608-612 ◽  
Author(s):  
Hiroshi Ito ◽  
Kazuhiro Takahashi ◽  
Jun Hatazawa ◽  
Seong-Gi Kim ◽  
Iwao Kanno

The hemodynamic mechanism of increase in cerebral blood flow (CBF) during neural activation has not been elucidated in humans. In the current study, changes in both regional CBF and cerebral blood volume (CBV) during visual stimulation in humans were investigated. Cerebral blood flow and CBV were measured by positron emission tomography using H215O and 11CO, respectively, at rest and during 2-Hz and 8-Hz photic flicker stimulation in each of 10 subjects. Changes in CBF in the primary visual cortex were 16% ± 16% and 68% ± 20% for the visual stimulation of 2 Hz and 8 Hz, respectively. The changes in CBV were 10% ± 13% and 21% ± 5% for 2-Hz and 8-Hz stimulation, respectively. Significant differences between changes in CBF and CBV were observed for visual stimulation of 8 Hz. The relation between CBF and CBV values during rest and visual stimulation was CBV = 0.88CBF0.30. This indicates that when the increase in CBF during neural activation is great, that increase is caused primarily by the increase in vascular blood velocity rather than by the increase in CBV. This observation is consistent with reported findings obtained during hypercapnia.


2003 ◽  
Vol 23 (6) ◽  
pp. 665-670 ◽  
Author(s):  
Hiroshi Ito ◽  
Iwao Kanno ◽  
Masanobu Ibaraki ◽  
Jun Hatazawa ◽  
Shuichi Miura

Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF. The relation between changes in CBF and cerebral blood volume (CBV) during hypercapnia and hypocapnia in humans, however, is not clear. Both CBF and CBV were measured at rest and during hypercapnia and hypocapnia in nine healthy subjects by positron emission tomography. The vascular responses to hypercapnia in terms of CBF and CBV were 6.0 ± 2.6%/mm Hg and 1.8 ± 1.3%/mm Hg, respectively, and those to hypocapnia were −3.5 ± 0.6%/mm Hg and −1.3 ± 1.0%/mm Hg, respectively. The relation between CBF and CBV was CBV = 1.09 CBF0.29. The increase in CBF was greater than that in CBV during hypercapnia, indicating an increase in vascular blood velocity. The degree of decrease in CBF during hypocapnia was greater than that in CBV, indicating a decrease in vascular blood velocity. The relation between changes in CBF and CBV during hypercapnia was similar to that during neural activation; however, the relation during hypocapnia was different from that during neural deactivation observed in crossed cerebellar diaschisis. This suggests that augmentation of CBF and CBV might be governed by a similar microcirculatory mechanism between neural activation and hypercapnia, but diminution of CBF and CBV might be governed by a different mechanism between neural deactivation and hypocapnia.


1987 ◽  
Vol 7 (4) ◽  
pp. 421-426 ◽  
Author(s):  
W. R. Wayne Martin ◽  
William J. Powers ◽  
Marcus E. Raichle

Local cerebral blood volume (CBV) has been measured previously with inhaled 11CO and positron emission tomography (PET). The model used assumes that equilibrium in tracer concentration has occurred between arterial and systemic venous blood before the PET measurement is made. To verify that this model may be used with the much shorter half-lived C15O, we have simultaneously measured arterial and venous blood radioactivity following C15O inhalation. Equilibrium occurred 95 ± 39 s after inhalation (n = 7). If the PET measurement is commenced prior to arteriovenous equilibrium, significant errors occur in calculated CBV. These data indicate that C15O may be used as a tracer for CBV measurement provided that emission data collection commences at ∼120 s after inhalation. Strict quality control measures must be maintained to minimize the contamination of administered C15O with 15O-labeled CO2.


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