Cerebral Blood Flow and Oxygen Consumption in the Rat Brain during Extreme Hypercarbia

Berntman, Leif; Dahlgren, Nils; Siesjö, Bo K.

doi:10.1097/00000542-197904000-00004

Cited by 67 publications

(21 citation statements)

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“…Despite the significant methodological differences between these studies and our own, which could have contributed to hemodynamic and metabolic disparities (Berntman et al, 1979;Keyeux et al, 1995), we wished to assess the sensitivity of our results to assumptions made regarding Ψ. An Ψ variation between −0.25 (Zappe et al, 2008) and 0.16 (Jones et al, 2005) would accommodate the observations of most deviations found in animal studies, and the corresponding power-law fits yielded α = 0.23 ± 0.03 (p b 0.001) and α = 0.17 ± 0.02 (p b 0.001).…”

Section: Resultsmentioning

confidence: 65%

MRI measurement of the BOLD-specific flow–volume relationship during hypercapnia and hypocapnia in humans

2010

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Section: Resultsmentioning

confidence: 65%

MRI measurement of the BOLD-specific flow–volume relationship during hypercapnia and hypocapnia in humans

2010

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“…The extracted NT-CNP was added to primary rabbit antiserum (J39) raised against NT-proCNP-(1-15) (1:6,000 dilution, 100 l antiserum/assay tube). Peptide standards were made from synthetic human proCNP- (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15), with the purity data supplied by the manufacturer (Chiron Technologies) taken into account. Within-and between-assay CVs were 6.0% and 7.9%, respectively.…”

Section: Analytic Measurementsmentioning

confidence: 99%

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

Peebles

Richards²,

Celi

et al. 2008

Journal of Applied Physiology

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Evidence from animal studies indicates that various vasoactive factors, including release of norepinephrine, endothelin, adrenomedullin, C-natriuretic peptide (CNP), and nitric oxide (NO), may play a role in arterial blood gas-induced alterations in CBF. For the first time, we directly quantified exchange of these vasoactive factors across the human brain. Using the Fick principle and transcranial Doppler ultrasonography, we measured CBF in 12 healthy humans at rest and during hypercapnia (4 and 8% CO 2), hypocapnia (voluntary hyperventilation), and hypoxia (12 and 10% O 2). At each level, blood was sampled simultaneously from the internal jugular vein and radial artery. With the exception of CNP and NO, the simultaneous quantification of norepinephrine, endothelin, or adrenomedullin showed no cerebral uptake or release during changes in arterial blood gases. Hypercapnia, but not hypocapnia, increased CBF and caused a net cerebral release of nitrite (a marker of NO), which was reflected by an increase in the venous-arterial difference for nitrite: 57 Ϯ 18 and 150 Ϯ 36 mol/l at 4% and 8% CO 2, respectively (both P Ͻ 0.05). Release of cerebral CNP was also observed during changes in CO 2 (hypercapnia vs. hypocapnia, P Ͻ 0.05). During hypoxia, there was a net cerebral uptake of nitrite, which was reflected by a decreased venous-arterial difference for nitrite: Ϫ96 Ϯ 14 mol/l at 10% O 2 (P Ͻ 0.05). These data indicate that there is a differential exchange of NO across the brain during hypercapnia and hypoxia and that CNP may play a complementary role in CO 2-induced CBF changes. cerebral circulation; nitric oxide; endothelium RESPIRATORY-INDUCED CHANGES in arterial PCO 2 (Pa CO 2 ) and, to a lesser extent, PO 2 (Pa O 2 ) play a major role in cerebral blood flow (CBF) regulation (9). Elevations in Pa CO 2 (hypercapnia) lead to vasodilation of cerebral arterioles in the downstream bed and a subsequent increase in CBF, whereas a reduction in Pa CO 2 (hypocapnia) leads to vasoconstriction and a subsequent decrease in CBF (28, 65). A fall in Pa O 2 (hypoxia) below a certain threshold (Ͻ40 Torr) also produces cerebral vasodilation (19). These arterial blood gas-induced changes in CBF are mediated through changes in cerebrovascular resistance via alterations in vascular smooth muscle diameter in response to changes in the level of intracellular calcium and/or calcium sensitivity (for review see Ref. 22). Cerebrovascular tone is influenced by several chemical substances, including nitric oxide (NO). NO, synthesized from the terminal guanidino nitrogen atom(s) of L-arginine in a two-step reaction that is catalyzed by the enzyme NO synthase (NOS) (48), is an important vasoactive factor that dilates the cerebral vasculature. Under normal conditions, two isoforms of NOS are expressed in the brain, endothelium-derived NOS (eNOS) and neuronal-derived NOS (nNOS) (61), although evidence for the role of eNOS vs. nNOS in the control of CBF is controversial (3). Vasodilation evoked by NO is initiated by an increase in cGMP (7).Pharmac...

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“…Since cerebral blood volume (CBV) is quantitatively correlated with arterial PCS (18), these results suggest the possibility of measuring CBV using susceptibility-based MR contrast.…”

Section: Introductionmentioning

confidence: 97%

MR Contrast Due to Microscopically Heterogeneous Magnetic Susceptibility: Numerical Simulations and Applications to Cerebral Physiology

Fisel

Ackerman

Buxton

et al. 1991

Magnetic Resonance in Med

329

182

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We calculate the effects of subvoxel variations in magnetic susceptibility on MR image intensity for spin-echo (SE) and gradient-echo (GE) experiments for a range of microscopic physical parameters. The model used neglects the overlap of gradients from one magnetic inclusion to the next, and so is valid for low volume fractions and weak perturbations of the magnetic field. Transverse relaxation is predicted to deviate significantly from linear exponential decay in both SE and GE at a particle radius of 2.5 microns. Calculated changes in transverse relaxation rates for SE and GE increase linearly with volume fraction of high-susceptibility regions of 5 microns diameter, but increase with about the 3/2 power of volume fraction of regions with 15 micron spacing between centers. This sensitivity to the actual size and spacing of magnetized regions may allow them to be measured on the basis of contrast. without being resolved in images. GE and SE decay rates are approximately twice as sensitive to long cylinders of 5 microns diameter than to spheres of the same size, for diffusion constants of 2.5 micron 2/ms. Calculated changes in transverse decay rates increase with approximately the square of field and susceptibility variation for 5-microns spheres and a diffusion constant of 2.5 microns 2/ms. This exponent is smaller for cylindrical magnetized regions of the same size, and also depends on the diffusion constant. We discuss possible applications of our theoretical results to the analysis of the effects of high-susceptibility contrast agents in brain. Experimental data from the literature are compared with calculated signal changes according to the model. The monotonic dependence of decay rates on the volume of distribution of the contrast agent suggests that cerebral blood volume and flow could be measured using MR contrast.

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Cerebral Blood Flow and Oxygen Consumption in the Rat Brain during Extreme Hypercarbia

Cited by 67 publications

References 0 publications

MRI measurement of the BOLD-specific flow–volume relationship during hypercapnia and hypocapnia in humans

MRI measurement of the BOLD-specific flow–volume relationship during hypercapnia and hypocapnia in humans

Human cerebral arteriovenous vasoactive exchange during alterations in arterial blood gases

MR Contrast Due to Microscopically Heterogeneous Magnetic Susceptibility: Numerical Simulations and Applications to Cerebral Physiology

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