Effects of insulin on hexose transport across blood-brain barrier in normoglycemia

1987 ◽  
Vol 252 (3) ◽  
pp. E299-E303 ◽  
Author(s):  
H. Namba ◽  
G. Lucignani ◽  
A. Nehlig ◽  
C. Patlak ◽  
K. Pettigrew ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Rate Constants ◽  
Time Course ◽  
Brain Barrier ◽  
Tissue Concentrations ◽  
Arterial Blood ◽  
Blood Brain ◽  
Measured Time ◽  
Time Courses ◽  
Arterial Plasma

The effects of insulin on 3-O-[14C]methylglucose transport across the blood-brain barrier (BBB) were studied in conscious rats under steady-state normoglycemic conditions. The [14C]methylglucose was infused intravenously at a constant rate, and animals were killed at various times between 5 and 30 min after the initiation of the infusion. The time course of the arterial plasma concentration of [14C]methylglucose was determined in timed arterial blood samples taken during the infusion. Local cerebral tissue concentrations of [14C]methylglucose at the time of killing were determined by quantitative autoradiography of brain sections. The rate constants for inward and outward transport of [14C]methylglucose across the BBB, K1, and k2, respectively, were estimated by a least-squares, best-fit of a kinetic equation to the measured time courses of plasma and tissue concentrations. K1 and k2 were reduced by an average of 24 and 31%, respectively, in gray matter and 7 and 16% in white matter from values estimated similarly in normal insulinemic control rats. The equilibrium distribution ratio, K1/k2, for [14C]methylglucose in brain increased by approximately 10–11% in the hyperinsulinemic animals. Because 3-O-[14C]methylglucose shares the same carrier that transports glucose and other hexoses across the BBB, these results suggest that hyperinsulinemia decreases the rate constants for transport but increases the distribution space for hexoses in brain. These effects are, however, quite small and are probably minor or negligible when compared with the major effects of insulin in other tissues.

The Distribution and Kinetics of [18F]6-Fluoro-3-O-Methyl-l-Dopa in the Human Brain

1994 ◽  
Vol 14 (4) ◽  
pp. 664-670 ◽  
Author(s):  
Lindi Wahl ◽  
Raman Chirakal ◽  
Gunter Firnau ◽  
E. Stephen Garnett ◽  
Claude Nahmias
Keyword(s):  
Blood Brain Barrier ◽  
Time Course ◽  
Nonhuman Primates ◽  
Dopamine Metabolism ◽  
Brain Barrier ◽  
Blood Brain ◽  
Measured Time ◽  
Bidirectional Transport ◽  
Kinetics Of ◽  
The Brain

The analysis of positron tomographic studies of 3,4-dihydroxyphenylethylamine (dopamine) metabolism in which [18F]6-fluoro-l-3,4-dihydroxyphenylalanine (F-dopa) is used as a tracer is confounded by the presence of [18F]6-fluoro-3- O-methyl-l-3,4-dihydroxyphenylalanine (OMFD). This labeled molecule, formed by the action of peripheral cathechol- O-methyltransferase on F-dopa, crosses the blood–brain barrier and contributes to the radioactivity measured by the tomograph. Corrections for this radioactivity in the brain have been proposed. They rely upon the assumption that regional variations in the handling of this molecule by the brain are negligible. Although this assumption is pivotal for the proper quantification of dopamine metabolism using F-dopa, the distribution and kinetics of OMFD have never been studied in humans. We present results in humans that show that there is little selective regional 18F accumulation in the brain, that the distribution volume of OMFD is close to unity, and that a single, reversible compartment is adequate to model the measured time course of radioactivity after an OMFD injection. Analysis of plasma samples for labeled metabolites showed that more than 95% of the radioactivity was associated with OMFD at all times. Our results for OMFD kinetics are in accord with published results obtained in nonhuman primates and for the bidirectional transport of large neutral amino acids across the blood-brain barrier measured using a synthetic amino acid. However, our results also indicate that there are small but significant differences in OMFD kinetics in different parts of the brain that may prevent inferences about the handling of OMFD in one part of the brain from being extended to other parts of the brain.

Time courses of changes in cerebral blood flow and blood-brain barrier integrity by focal proton radiation in the rat

1996 ◽  
Vol 18 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Hiroki Namba ◽  
Toshiaki Irie ◽  
Kiyoshi Fukushi ◽  
Masaomi lyo ◽  
Takahiro Hashimoto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Proton Radiation ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Time Courses ◽  
Blood Brain Barrier Integrity

scholarly journals Slowly Changing Bioelectric Potentials Associated With the Blood-Brain Barrier

1958 ◽  
Vol 195 (1) ◽  
pp. 7-22 ◽  
Author(s):  
Robert D. Tschirgi ◽  
J. Langdon Taylor
Keyword(s):  
Cerebral Cortex ◽  
Blood Brain Barrier ◽  
Interstitial Fluid ◽  
Brain Barrier ◽  
Membrane Diffusion ◽  
Arterial Blood ◽  
Blood Ph ◽  
Blood Brain ◽  
The Central Nervous System ◽  
Bioelectric Potentials

A slowly changing bioelectric potential difference (P.D.) is measured in rats, rabbits, cats and dogs between various regions of the central nervous system (CNS) and the blood within the jugular vein. It is shown that the CNS-blood P.D. is very sensitive to alterations in alveolar CO2 tension, but this relationship is dependent upon the H+ concentration rather than CO2 per se. Whereas increasing intravenous H+ concentration increases CNS positivity, topical application of acid solutions directly to the cerebral cortex decreases CNS positivity. The same relationship is found for intravenous and topical K+. Anoxia and circulatory failure produce CNS negative deflections, often exceeding 15 mv, which do not return to zero for over 24 hours after death. Simultaneous measurements of arterial blood pH, cerebral cortex pH and CNS-blood P.D. reveal the following relationship among these variables: ΔP.D. = κ Δ log10 [H+]a/[H+]i where [H+]a is the H+ concentration of the arterial blood and [H+]i is the H+ concentration of the CNS interstitial fluid. For the CNS-blood P.D. between cerebral cortex and jugular blood of rabbits and rats, κ is found to be 29 ± 5. These results are interpreted as indicating a source of emf across the pan-vascular blood-brain barrier which resembles a membrane diffusion potential. The blood-brain barrier is postulated to be more permeable to H+ and K+ than to anions and other cations.

Time Course and Size of Blood–Brain Barrier Opening in a Mouse Model of Blast-Induced Traumatic Brain Injury

2016 ◽  
Vol 33 (13) ◽  
pp. 1202-1211 ◽  
Author(s):  
Christopher D. Hue ◽  
Frances S. Cho ◽  
Siqi Cao ◽  
Russell E. Nicholls ◽  
Edward W. Vogel III ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mouse Model ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Brain Barrier ◽  
Blood Brain ◽  
Barrier Opening ◽  
Blood Brain Barrier Opening

scholarly journals Effect of the Calcium Antagonist, Nimodipine, on Cerebral Blood Flow and Metabolism in the Primate

1981 ◽  
Vol 1 (3) ◽  
pp. 349-356 ◽  
Author(s):  
A. M. Harper ◽  
L. Craigen ◽  
S. Kazda
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Calcium Antagonist ◽  
Arterial Blood Pressure ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Arterial Blood ◽  
Blood Brain ◽  
Significant Change

The effect of the calcium antagonist nimodipine was tested in anaesthetised primates. A rapid intravenous injection of 3 or 10 μg kg−1 produced a transient rise in end-tidal Pco2 and a fall in arterial blood pressure, but 10 min after the injection there was no significant change in CBF. A continuous intravenous infusion of 2 μg kg−1 min−1 caused a modest fall in mean arterial blood pressure and an increase in cerebral blood flow (CBF), which gradually increased to 27% above control after 50 min infusion. There was no significant change in CMRO2. A continuous intracarotid infusion of 0.67 μg kg−1 min−1 caused an increase in CBF of between 46 and 57%. This was further increased to 87% above control after disruption of the blood-brain barrier with hyperosmolar urea. Thirty minutes after the urea, the CBF returned to 43% above control. Twenty minutes after the infusion of nimodipine had been stopped, the CBF had returned to control values. EEG studies in this group showed no obvious increase in electrocortical activity. This evidence suggests that nimodipine has no effect on cerebral metabolism but increases CBF, particularly after disruption of the blood-brain barrier.

scholarly journals Immunolocalization of Heat Shock Protein after Fluid Percussive Brain Injury and Relationship to Breakdown of the Blood-Brain Barrier

1993 ◽  
Vol 13 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Hirokazu Tanno ◽  
Russ P. Nockels ◽  
Lawrence H. Pitts ◽  
Linda J. Noble
Keyword(s):  
Brain Injury ◽  
Head Injury ◽  
Blood Vessels ◽  
Blood Brain Barrier ◽  
Time Course ◽  
Cortical Layer ◽  
Brain Barrier ◽  
Impact Site ◽  
Blood Brain ◽  
The Impact

We have previously developed a model of mild, lateral fluid percussive head injury in the rat and demonstrated that although this injury produced minimal hemorrhage, breakdown of the blood–brain barrier was a prominent feature. The relationship between posttraumatic blood–brain barrier disruption and cellular injury is unclear. In the present study we examined the distribution and time course of expression of the stress protein HSP72 after brain injury and compared these findings with the known pattern of breakdown of the blood–brain barrier after a similar injury. Rats were subjected to a lateral fluid percussive brain injury (4.8–5.2 atm, 20 ms) and killed at 1, 3, and 6 h and 1,3, and 7 days after injury. HSP72-like immunoreactivity was evaluated in sections of brain at the light-microscopic level. The earliest expression of HSP72 occurred at 3 h postinjury and was restricted to neurons and glia in the cortex surrounding a necrotic area at the impact site. By 6 h, light immunostaining was also noted in the pia-arachnoid adjacent to the impact site and in certain blood vessels that coursed through the area of necrosis. Maximal immunostaining was observed by 24 h postinjury, and was primarily associated with the cortex immediately adjacent to the region of necrosis at the impact site. This region consisted of darkly immunostained neurons, glia, and blood vessels. Immunostaining within the region of necrosis was restricted to blood vessels. HSP72-like immunoreactivity was also noted in a limited number of neurons and glia in other brain regions, including the parasagittal cortex, deep cortical layer VI, and CA3 in the posterior hippocampus. Immunoreactive cells in these areas were not apparent until 24 h postinjury. By 7 days postinjury, HSP72-like immunoreactivity was minimal or absent in these injured brains and notable cell loss was apparent only in the impact site. This study demonstrates an early and pronounced expression of HSP72 at the impact site and a more delayed and less prominent expression of this protein in other regions of the brain. These findings parallel the temporal and regional pattern of breakdown of the blood–brain barrier after a similar head injury.

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