scholarly journals Blood-Brain Barrier Transport and Brain Metabolism of Glucose during Acute Hyperglycemia in Humans1

2001 ◽  
Vol 86 (5) ◽  
pp. 1986-1990
Author(s):  
Steen G. Hasselbalch ◽  
Gitte M. Knudsen ◽  
Brunella Capaldo ◽  
Alfredo Postiglione ◽  
Olaf B. Paulson
Keyword(s):  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Human Subjects ◽  
Brain Barrier ◽  
Indicator Method ◽  
Acute Hyperglycemia ◽  
Blood Brain ◽  
18F Fluorodeoxyglucose ◽  
Positron Emission ◽  
Area Product

It is controversial whether transport adaptation takes place in chronic or acute hyperglycemia. Blood-brain barrier glucose permeability and regional brain glucose metabolism (CMRglc) was studied in acute hyperglycemia in six normal human subjects (mean age, 23 yr) using the double indicator method and positron emission tomography and[ 18F]fluorodeoxyglucose as tracer. The Kety-Schmidt technique was used for measurement of cerebral blood flow (CBF). After 2 h of hyperglycemia (15.7 ± 0.7 mmol/L), the glucose permeability-surface area product from blood to brain remained unchanged (0.050 ± 0.008 vs. 0.059 ± 0.031 mL/100 g·min). The unidirectional clearance of[ 18F]fluorodeoxyglucose (K1*) was reduced from 0.108 ± 0.011 to 0.061 ± 0.005 mL/100 g·min (P < 0.0004). During hyperglycemia, global CMRglc remained constant (21.4 ± 1.2 vs. 23.1 ± 2.2 μmol/100 g·min, normo- and hyperglycemia, respectively). Except for a significant increase in white matter CMRglc, no regional difference in CMRglc was found. Likewise, CBF remained unchanged. The reduction in K1* was compatible with Michaelis-Menten kinetics for facilitated transport. Our findings indicate no major adaptational changes in the maximal transport velocity or affinity to the blood-brain barrier glucose transporter. Finally, hyperglycemia did not change global CBF or CMRglc.

scholarly journals Measurement of Blood—Brain Barrier Permeability with Positron Emission Tomography and [68Ga]EDTA

1984 ◽  
Vol 4 (3) ◽  
pp. 323-328 ◽  
Author(s):  
R. M. Kessler ◽  
J. C. Goble ◽  
J. H. Bird ◽  
M. E. Girton ◽  
J. L. Doppman ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Brain Barrier ◽  
Quantitative Measure ◽  
Brain Regions ◽  
Emission Tomography ◽  
Brain Barrier ◽  
Blood Brain ◽  
Positron Emission ◽  
Area Product

Positron emission tomography (PET) was employed to examine time-dependent changes in blood–brain barrier (BBB) permeability to [68Ga]ethylenediaminetetraacetate (EDTA) in the rhesus monkey, following reversible barrier opening by intracarotid infusion of a hypertonic mannitol solution. The PET technique, when combined with measurements of plasma radioactivity, provided a quantitative measure of the cerebrovascular permeability-area product ( PA) at different times following mannitol infusion. Hypertonic mannitol treatment reversibly increased PA to [68Ga]EDTA more than 10-fold; much of the barrier effect was over by 10 min after mannitol treatment. The results show that PET can be used to measure transient changes in BBB integrity in specific brain regions, under in vivo, noninvasive conditions.

Acute upregulation of blood-brain barrier glucose transporter activity in seizures

2000 ◽  
Vol 279 (3) ◽  
pp. H1346-H1354 ◽  
Author(s):  
Eain M. Cornford ◽  
Eddy V. Nguyen ◽  
Elliot M. Landaw
Keyword(s):  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Brain Barrier ◽  
Brain Extraction ◽  
Blood Brain ◽  
Half Saturation Constant ◽  
Permeability Surface ◽  
Permeability Increase ◽  
Cortical Regions ◽  
Area Product

Brain extraction of 18F-labeled 2-fluoro-2-deoxy-d-glucose (FDG) was significantly higher in pentylene tetrazole (PTZ)-treated rats (32 ± 4%) than controls (25 ± 4%). The FDG permeability-surface area product ( PS) was also significantly higher with PTZ treatment (0.36 ± 0.05 ml · min−1 · g−1) than in controls (0.20 ± 0.06 ml · min−1 · g−1). Cerebral blood flow rates were also elevated by 50% in seizures. The internal carotid artery perfusion technique indicated mean [14C]glucose clearance (and extraction) was increased with PTZ treatment, and seizures increased the PS by 37 ± 16% ( P < 0.05) in cortical regions. Because kinetic analyses suggested the glucose transporter half-saturation constant ( K m) was unchanged by PTZ, we derived estimates of 1) treated and 2) control maximal transporter velocities ( V max) and 3) a single K m. In cortex, the glucose transporter V max was 42 ± 11% higher ( P < 0.05) in PTZ-treated animals (2.46 ± 0.34 μmol · min−1 · g−1) than in control animals (1.74 ± 0.26 μmol · min−1 · g−1), and the K m = 9.5 ± 1.6 mM. Blood-brain barrier (BBB) V max was 31 ± 10% greater ( P < 0.05) in PTZ-treated (2.36 ± 0.30 μmol · min−1 · g−1) than control subcortex (1.80 ± 0.25 μmol · min−1 · g−1). We conclude acute upregulation of BBB glucose transport occurs within 3 min of an initial seizure. Transporter V max and BBB glucose permeability increase by 30–40%.

Hyperosmolar blood-brain barrier disruption in baboons: an in vivo study using positron emission tomography and rubidium-82

1996 ◽  
Vol 84 (3) ◽  
pp. 494-502 ◽  
Author(s):  
Bernhard Zünkeler ◽  
Richard E. Carson ◽  
Jeffrey Olson ◽  
Ronald G. Blasberg ◽  
Mary Girton ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Brain Tumors ◽  
Blood Brain Barrier ◽  
Emission Tomography ◽  
Brain Barrier ◽  
Blood Brain ◽  
Positron Emission ◽  
The Mean ◽  
Rubidium 82

✓ Hyperosmolar blood-brain barrier (BBB) disruption remains controversial as an adjuvant therapy to increase delivery of water-soluble compounds to extracellular space in the brain in patients with malignant brain tumors. To understand the physiological effects of BBB disruption more clearly, the authors used positron emission tomography (PET) to study the time course of BBB permeability in response to the potassium analog rubidium-82 (82Rb, halflife 75 seconds) following BBB disruption in anesthetized adult baboons. Mannitol (25%) was injected into the carotid artery and PET scans were performed before and serially at 8- to 15-minute intervals after BBB disruption. The mean influx constant (K1), a measure of permeability-surface area product, in ipsilateral, mannitol-perfused mixed gray- and white-matter brain regions was 4.9 ± 2.4 µl/min/ml (± standard deviation) at baseline and increased more than 100% (ΔK1 = 9.4 ± 5.1 µl/min/ml, 18 baboons) in brain perfused by mannitol. The effect of BBB disruption on K1 correlated directly with the total amount of mannitol administered (p < 0.005). Vascular permeability returned to baseline with a halftime of 24.0 ± 14.3 minutes. The mean brain plasma volume rose by 0.57 ± 0.34 ml/100 ml in ipsilateral perfused brain following BBB disruption. This work provides a basis for the in vivo study of permeability changes induced by BBB disruption in human brain and brain tumors.

Glucose transport by isolated plasma membranes of the bovine blood-brain barrier

1997 ◽  
Vol 272 (5) ◽  
pp. C1552-C1557 ◽  
Author(s):  
W. J. Lee ◽  
D. R. Peterson ◽  
E. J. Sukowski ◽  
R. A. Hawkins
Keyword(s):  
Glucose Transport ◽  
Blood Brain Barrier ◽  
Plasma Membranes ◽  
Glucose Transporter ◽  
Extracellular Fluid ◽  
Brain Barrier ◽  
Maximal Velocity ◽  
Plasma Membrane Vesicles ◽  
Cerebral Microvessels ◽  
Blood Brain

Luminal and abluminal endothelial plasma membrane vesicles were isolated from bovine cerebral microvessels, the site of the blood-brain barrier. Glucose transport across each membrane was measured using a rapid-filtration technique. Glucose transport into luminal vesicles occurred by a stereospecific energy-independent transporter [Michaelis-Menten constant (K(m)) = 10.3 +/- 2.8 (SE) mM and maximal velocity (Vmax) = 8.6 +/- 2.0 nmol.mg protein(-1).min-1]. Kinetic analysis of abluminal vesicles also showed a transport system with characteristics similar to the luminal transporter (K(m) = 12.5 +/- 2.3 mM and Vmax = 10.0 +/- 1.0 nmol.mg protein-1.min-1). These functional, facilitative glucose transporters were symmetrically distributed between the luminal and abluminal membrane domains, providing a mechanism for glucose movement between blood and brain. The studies also revealed a Na-dependent transporter on the abluminal membrane with a higher affinity and lower capacity than the facilitative transporters (K(m) = 130 +/- 20 microM and Vmax = 1.59 +/- 0.44 nmol.mg protein-1.min-1. The abluminal Na-dependent glucose transporter is in a position to transport glucose from the brain extracellular fluid into the endothelial cells of the blood-brain barrier. The functional significance of its presence there remains to be determined.

scholarly journals Approaching Complete Inhibition of P-Glycoprotein at the Human Blood–Brain Barrier: An (R)-[11C]Verapamil PET Study

2015 ◽  
Vol 35 (5) ◽  
pp. 743-746 ◽  
Author(s):  
Martin Bauer ◽  
Rudolf Karch ◽  
Markus Zeitlinger ◽  
Cécile Philippe ◽  
Kerstin Römermann ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Brain Barrier ◽  
Distribution Volume ◽  
Emission Tomography ◽  
Brain Barrier ◽  
Whole Brain ◽  
P Glycoprotein ◽  
Blood Brain ◽  
Positron Emission ◽  
Pet Scans

As P-glycoprotein (Pgp) inhibition at the blood–brain barrier (BBB) after administration of a single dose of tariquidar is transient, we performed positron emission tomography (PET) scans with the Pgp substrate ( R)-[11C]verapamil in five healthy volunteers during continuous intravenous tariquidar infusion. Total distribution volume ( VT) of ( R)-[11C]verapamil in whole-brain gray matter increased by 273 ± 78% relative to baseline scans without tariquidar, which was higher than previously reported VT increases. During tariquidar infusion whole-brain VT was comparable to VT in the pituitary gland, a region not protected by the BBB, which suggested that we were approaching complete Pgp inhibition at the human BBB.

Effects of Acute Hyperglycemia on Blood Brain Barrier During Pentylenetetrazole-induced Epileptic Seizures

2012 ◽  
Vol 8 (6) ◽  
pp. 561-566 ◽  
Author(s):  
Hatice Yorulmaz ◽  
F. Burcu Seker ◽  
Baria Oztas ◽  
Engin Kaptan ◽  
Kursat Ozdilli
Keyword(s):  
Blood Brain Barrier ◽  
Epileptic Seizures ◽  
Brain Barrier ◽  
Acute Hyperglycemia ◽  
Blood Brain
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