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At least 1,243 records · Page 69Linked to original sources
PubMed2006

Effects of fractionated radiation on the brain vasculature in a murine model: blood-brain barrier permeability, astrocyte proliferation, and ultrastructural changes.

PURPOSE: Radiation therapy of CNS tumors damages the blood-brain barrier (BBB) and normal brain tissue. Our aims were to characterize the short- and long-term effects of fractionated radiotherapy (FRT) on cerebral microvasculature in mice and to investigate the mechanism of change in BBB permeability in mice. METHODS AND MATERIALS: Intravital microscopy and a cranial window technique were used to measure BBB permeability to fluorescein isothiocyanate (FITC)-dextran and leukocyte endothelial interactions before and after cranial irradiation. Daily doses of 2 Gy were delivered 5 days/week (total, 40 Gy). We immunostained the molecules to detect the expression of glial fibrillary acidic protein and to demonstrate astrocyte activity in brain parenchyma. To relate the permeability changes to endothelial ultrastructural changes, we used electron microscopy. RESULTS: Blood-brain barrier permeability did not increase significantly until 90 days after FRT, at which point it increased continuously until 180 days post-FRT. The number of adherent leukocytes did not increase during the study. The number of astrocytes in the cerebral cortex increased significantly; vesicular activity in endothelial cells increased beginning 90 days after irradiation, and most tight junctions stayed intact, although some were shorter and less dense at 120 and 180 days. CONCLUSIONS: The cellular and microvasculature response of the brain to FRT is mediated through astrogliosis and ultrastructural changes, accompanied by an increase in BBB permeability. The response to FRT is delayed as compared with single-dose irradiation treatment, and does not involve leukocyte adhesion. However, FRT induces an increase in the BBB permeability, as in the case of single-dose irradiation.

Animals↗
PubMed2004

Method for measurement of the blood-brain barrier permeability in the perfused mouse brain: application to amyloid-beta peptide in wild type and Alzheimer's Tg2576 mice.

The role of transport exchanges of neuroactive solutes across the blood-brain barrier (BBB) is increasingly recognized. To take full advantage of genetically altered mouse models of neurodegenerative disorders for BBB transport studies, we adapted a brain perfusion technique to the mouse. During a carotid brain perfusion with a medium containing sheep red blood cells and mock plasma, the physiological parameters in the arterial inflow, regional cerebral blood flow (14C-iodoantipyrine autoradiography), ultrastructural integrity of the tissue, barrier to lanthanum, brain water content, energy metabolites and lactate levels remain unchanged. Amyloid-beta peptides (Abeta) were iodinated by lactoperoxidase method. Non-oxidized mono-iodinated Abeta monomers were separated by HPLC (as confirmed by MALDI-TOF spectrometry) and used in transport measurements. Transport of intact 125I-Abeta40 across the BBB was time- and concentration-dependent in contrast to negligible 14C-inulin uptake. In 5-6 months old Alzheimer's Tg2576 mice, Abeta40 BBB transport was increased by >eight-fold compared to age-matched littermate controls, and was mediated via the receptor for advanced glycation endproducts. We conclude the present arterial brain perfusion method provides strictly controlled environment in cerebral microcirculation suitable for examining transport of rapidly and slowly penetrating molecules across the BBB in normal and transgenic mice.

Adenosine Triphosphate↗
PubMed1988

Regional distribution of immunoreactive brain natriuretic peptide in porcine brain and spinal cord.

In order to elucidate the physiological functions of brain natriuretic peptide (BNP), radioimmunoassay for BNP was established and regional distribution of BNP in porcine brain and spinal cord was investigated. The concentration of immunoreactive (ir-) BNP in porcine whole brain was estimated to be 0.63 pmol/g, 13 times higher than that of ir-atrial natriuretic peptide (ANP). Highest concentrations of ir-BNP were found in the medulla-pons, striatum, and spinal cord. Medium concentration was noted in the hypothalamus. This distribution of ir-BNP in porcine brain was found to be different from that of ir-ANP simultaneously measured. Furthermore, BNP and BNP-32 were identified as two major forms of ir-BNP in porcine brain.

Amino Acid Sequence↗
PubMed2002

Aluminum citrate uptake by immortalized brain endothelial cells: implications for its blood-brain barrier transport.

The objective was to further test the hypothesis that aluminum (Al) citrate transport across the blood-brain barrier is mediated by a monocarboxylate transporter (MCT). Speciation calculations showed that Al citrates were the predominant Al species under the conditions employed. Al citrate did not inhibit lactate uptake and was not taken up by the rat erythrocyte, suggesting it does not serve as an effective substrate for either MCT1 or the anion exchanger. Studies were conducted with b.End5 cells derived from mouse brain endothelial cells to identify the properties of the carrier(s) mediating Al citrate transport. Western blot analysis of b.End5 cells showed expression of the transferrin receptor and MCT1, but not MCT2 or MCT4. Uptake of Al citrate was approximately 70% faster than citrate. Citrate and Al citrate uptake were sodium independent. Citrate uptake increased at pH 6.9 compared to 7.4, whereas Al citrate uptake did not. Al citrate uptake was reduced by inhibitors of mitochondrial respiration and oxidative phosphorylation, suggesting ATP dependence, but not by ouabain, suggesting no role for Na/K-ATPase. Uptake was not affected by alpha-ketoglutarate or malonate, substrates for the dicarboxylate carrier. Many substrates and inhibitors of MCT1 and organic anion transporters reduced Al citrate uptake into b.End5 cells. BSP and fluorescein, organic anion transporter substrates/inhibitors, inhibited Al citrate uptake. We conclude that Al citrate transport across the blood-brain barrier is carrier-mediated, involving either an uncharacterized MCT isoform expressed in the brain such as MCT7 or MCT8 and/or one of the many members of the organic anion transporting protein family, some of which are known to be expressed at the blood-brain barrier.

Aluminum↗
PubMed2003

Use of a three-dimensional in vitro model of the rat blood-brain barrier to assay nucleoside efflux from brain.

Extracellular adenosine is produced in brain during physiological and pathophysiological conditions. Once produced, this adenosine can undergo one or more of the following fates: it can interact with its receptors, it can be scavenged by astrocytes and/or neurons for ATP resynthesis, it can be transported across the blood-brain barrier and lost from the central nervous system, or it can be metabolized to inosine and hypoxanthine. The present study used a three-dimensional in vitro cell culture model of the rat blood-brain barrier, in which forebrain astrocytes and microvascular endothelial cells were cultured in cartridges containing multiple parallel polypropylene hollow fibers. Endothelial cells were cultured on the inner surfaces and astrocytes on the outer surfaces of these fibers. Growth medium was constantly perfused through the lumen of the fibers to mimic blood flow across endothelial cells in vivo. This co-culture system was used to examine the permeation of adenosine, and its metabolite inosine, from the astrocyte compartment to the endothelial cell compartment. Dipyridamole was added to the media perfusing the endothelial cell compartment to test whether it could decrease permeation of adenosine and inosine across the in vitro blood-brain barrier. Our results indicate that dipyridamole decreased permeation of total purines, especially inosine, across the barrier. Furthermore, permeation of fluorescein isothiocyanate-labeled albumin and radiolabeled sucrose, markers of the paracellular permeation pathway, were also decreased by dipyridamole. In conclusion, these data indicate that in addition to inhibiting nucleoside efflux across the barrier, dipyridamole can also improve blood-brain barrier function in this model.

Adenosine↗
PubMed1999

Effects of ethanol on brain lactate in experimental traumatic brain injury with hemorrhagic shock.

OBJECTIVE: Previous studies of traumatic brain injury (TBI) and hemorrhagic shock (HS) models, have shown cardiorespiratory depression in ethanol-treated animals. This study investigated the effects of ethanol (ET) on brain lactate concentrations and acidosis in a TBI/HS model. METHODS: Anesthetized swine were instrumented and subjected to injury (INJ) consisting of fluid percussion TBI of 3 atm with concurrent 30 ml/kg graded hemorrhage over 30 min. Three groups were studied: Sham, INJ and INJ/ET. ET was given preinjury as a 2-g/kg i.v. bolus over 30 min, and an infusion of 0.4 g kg(-1) h(-1). Cardiorespiratory and cerebral physiologic data were monitored continuously for 150 min postinjury. Cerebral and renal blood flow was measured with colored microspheres. Brains were frozen in situ with liquid nitrogen. Lactate was measured with an enzymatic method. RESULTS: ET levels at injury were 219+/-24 mg/dl. The INJ/ET group had increased mortality, impaired ventilation, and reduced renal blood flow. Brain (cortical) lactate levels were significantly higher and cerebral venous lactate concentrations were increased in the INJ/ET group during the postinjury period. Cerebral venous glucose was significantly higher in the INJ/ET group, and cerebral venous pH was significantly lower. CONCLUSION: In this TBI/HS model, ethanol-induced increases in lactate concentrations in brain tissue and cerebral venous blood are associated with respiratory depression and reduced organ blood flow.

Analysis of Variance↗
PubMed1998

Brain death and transcranial Doppler: experience in 130 cases of brain dead patients.

BACKGROUND AND PURPOSE: Diagnosis of brain death requires confirmation of the clinical diagnosis by appropriate tests, generally electroencephalography (EEG) and angiography. The diagnostic limitations or logistical problems inherent to these tests indicate the need to develop other more appropriate methods. The results obtained with transcranial Doppler (TCD) led us to conduct this prospective study of TCD recordings in brain dead patients. METHODS: 130 patients, aged 2-88 years were diagnosed as brain dead between July 1987 and June 1993. Clinical criteria were confirmed in all cases by EEG (n=88) and or angiography (n=64). Intracranial anterior circulation was insonated via temporal windows or, when impossible, via a transorbital approach. The posterior circulation was studied only in more recent patients. Examinations were made as soon as possible after brain death diagnosis and repeated for about 30 min. Vital parameters and treatments were taken into account. RESULTS: There was only one false negative result, in a patient with an extended skull defect, who retained TCD and angiographic intracranial circulation despite confirmed irreversible brain death. All other patients displayed typical ultrasonic patterns of cerebral circulation arrest: an oscillating signal (n= 190, 73%), a systolic spike (n=62, 24%) or a unilateral absence of signal (n=5). Despite a total correlation for positive diagnosis, TCD and angiography may differ as to the level of circulation arrest. TCD is useful for patients under sedative drugs. No false positive result was encountered but we were unable to insonate any intracranial artery in 5 patients. CONCLUSION: Data from previous studies and the results of this study indicate that TCD is a very sensitive and safe method for diagnosing cerebral circulatory arrest. TCD may be used as a confirmatory test alongside EEG and angiography. TCD is more widely applicable than EEG and may be earlier and safer than angiography.

Adolescent↗
PubMed2001

Diffuse brain injury induces local expression of Na+/myo-inositol cotransporter in the rat brain.

We studied expression of an osmoprotective gene, sodium/myo-inositol cotransporter (SMIT) in Marmarou's animal model for human diffuse brain injury by in situ hybridization and immunohistochemistry. In rats with diffuse brain injury, transient upregulation of SMIT mRNA was exclusively observed in the lateral area of pyramidal tract in lower brainstem. The expression was induced at 1 h after injury, peaked at 24 h, and returned to almost control levels at 48 h. Upregulated expression was found mainly in small glia-like cells. By immunohistochemistry using antibodies to phosphorylated mitogen-activated protein (MAP) kinases, inductions of phosphorylated p44/42 MAP kinase were also observed after diffuse brain injury. Interestingly, the distribution patterns of induced phosphorylated p44/42 MAP kinase were completely coincident with those of upregulated SMIT mRNA after diffuse brain injury. These results suggest that diffuse brain injury induces local expression of SMIT by activation of p44/42 MAP kinase cascade. The confined SMIT induction may reflect regional differences of damage and/or cellular differences in sensitivity to neuropathological stresses caused by this injury.

Animals↗
PubMed1997

Amelioration of brain edema by topical application of glial cell line-derived neurotrophic factor in reperfused rat brain.

Glial cell line-derived neurotrophic factor (GDNF) was applied topically on the brain surface of reperfused rat brain after 90 min of transient middle cerebral artery occlusion. In contrast to the cases treated with vehicle, a formation of brain edema was greatly reduced at 2 days by the treatment with GDNF. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) staining was also markedly reduced in the cases with GDNF treatment both at 1 and 2 days of reperfusion. However, amelioration of the induction of immunoreactive 70 kDa heat shock protein was only a minimum by the GDNF treatment. The present results suggest that the treatment with GDNF has a significant effect on ameliorating brain edema formation after transient focal brain ischemia, and the effect is greatly associated with the reduction of TUNEL staining, but minimally with that of stress response of cells.

Animals↗
PubMed1999

Effects of circulating tumor necrosis factor on the neuronal activity and expression of the genes encoding the tumor necrosis factor receptors (p55 and p75) in the rat brain: a view from the blood-brain barrier.

Tumor necrosis factor is a potent activator of myeloid cells, which acts via two cell-surface receptors, the p55 and p75 tumor necrosis factor receptors. The present study describes the cellular distribution of both receptor messenger RNAs across the rat brain under basal conditions and in response to systemic injection with the bacterial endotoxin lipopolysaccharide and recombinant rat tumor necrosis factor-alpha. Time-related induction of the messenger RNA encoding c-fos, cyclo-oxygenase-2 enzyme and the inhibitory factor kappa B alpha was assayed as an index of activated neurons and cells of the microvasculature by intravenous tumor necrosis factor-alpha challenge. The effect of the proinflammatory cytokine on the hypothalamic-pituitary-adrenal axis was determined by measuring the transcriptional activity of corticotropin-releasing factor and plasma corticosterone levels. Constitutive expression of p55 messenger RNA was detected in the circumventricular organs, choroid plexus, leptomeninges, the ependymal lining cells of the ventricular walls and along the blood vessels, whereas p75 transcript was barely detectable in the brain under basal conditions. Immunogenic insults caused up-regulation of both tumor necrosis factor receptors in barrier-associated structures, as well as over the blood vessels, an event that was associated with a robust activation of the microvasculature. Indeed, intravenous tumor necrosis factor-alpha provoked a rapid and transient transcription of inhibitory factor kappa B alpha and cyclo-oxygenase-2 within cells of the blood-brain barrier, and a dual-labeling technique provided the anatomical evidence that the endothelium of the brain capillaries expressed inhibitory factor kappa B alpha. Circulating tumor necrosis factor-alpha also rapidly stimulated c-fos expression in nuclei involved in the autonomic control, including the bed nucleus of the stria terminalis, the paraventricular nucleus of the hypothalamus, the central nucleus of the amygdala, the nucleus of the solitary tract and the ventrolateral medulla. A delayed c-fos mRNA induction was detected in the circumventricular organs, organum vascularis of the lamina terminalis, the subfornical organ, the median eminence and the area postrema. The paraventricular nucleus of the hypothalamus exhibited expression of corticotropin-releasing factor primary transcript that was associated with a sharp increase in the plasma corticosterone levels 1h after intravenous tumor necrosis factor-alpha administration. Taken together, these data provide the evidence that p55 is the most abundant tumor necrosis factor receptor in the central nervous system and is expressed in barrier-associated structures. Circulating tumor necrosis factor has the ability to directly activate the endothelium of the brain's large blood vessels and small capillaries, which may produce soluble molecules (such as prostaglandins) to vehicle the signal through parenchymal elements. The pattern of c-fos-inducible nuclei suggests complex neuronal circuits solicited by the cytokine to activate neuroendocrine corticotropin-releasing factor and the corticotroph axis, a key physiological response for the appropriate control of the systemic inflammatory response.

Animals↗
PubMed2003

Characterization of normal brain and brain tumor pathology by chisquares parameter maps of diffusion-weighted image data.

OBJECTIVE: To characterize normal and pathologic brain tissue by quantifying the deviation of diffusion-related signal from a simple monoexponential decay, when measured over a wider than usual range of b-factors. METHODS AND MATERIALS: Line scan diffusion imaging (LSDI), with diffusion weighting at multiple b-factors between 100 and 5000 s/mm(2), was performed on 1.5 T clinical scanners. Diffusion data of single slice sections were acquired in five healthy subjects and 19 brain tumor patients. In-patients, conventional T2-weighted and contrast-enhanced T1-weighted images were obtained for reference purposes. The chisquare (chi(2)) error parameter associated with the monoexponential fits of the measured tissue water signals was then used to quantify the departure from a simple monoexponential signal decay on a pixel-by-pixel basis. RESULTS: Diffusion-weighted images over a wider b-factor range than typically used were successfully obtained in all healthy subjects and patients. Normal and pathologic tissues demonstrated signal decays, which clearly deviate from a simple monoexponential behavior. The chi(2) of cortical and deep grey matter was considerably lower than in white matter. In peritumoral edema, however, chi(2) was 68% higher than in normal white matter. In highly malignant brain tumors, such as glioblastoma multiforme (GBM) or anaplastic astrocytoma, chi(2) values were on average almost 400% higher than in normal white matter, while for one low grade astrocytoma and two cases of metastasis, chi(2) was not profoundly different from the chi(2) value of white matter. Maps of the chi(2) values provide good visualization of spatial details. However, the tumor tissue contrast generated appeared in many cases to be different from the enhancement produced by paramagnetic contrast agents. For example, in cases where the contrast agent only highlighted the rim of the tumor, chi(2) enhancement was present within the solid part of the tumor. CONCLUSION: The deviation from a purely monoexponential diffusion signal decay becomes evident as diffusion encoding is extended well beyond the normal range. The chi(2) error parameter as a measure of this deviation seems to provide sufficient lesion contrast to permit differentiation of malignant brain tumors from normal brain tissue.

Adult↗
PubMed2003

Assessment of ESR-CT imaging by comparison with autoradiography for the distribution of a blood-brain-barrier permeable spin probe, MC-PROXYL, to rodent brain.

Blood-brain-barrier (BBB)-permeable, 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-1-yloxy (MC-PROXYL) and BBB-impermeable carbamoyl-PROXYL were used to assess the ESR imaging technique by comparing with autoradiography. For this purpose, spin probes, 14C-labeled at their five-membered ring, [14C]MC-PROXYL and [14C]carbamoyl-PROXYL, were newly synthesized. These probes were i.p. or i.v. injected into rats and autoradiograms were recorded. The autoradiograms of rat head showed that [14C]MC-PROXYL distributed well in the brain compared to [14C]carbamoyl-PROXYL. In vivo ESR spectra and two-dimensional ESR images of isolated rat brain treated with MC- or carbamoyl-PROXYL also indicated the extensive distribution of MC-PROXYL but not carbamoyl-PROXYL in the rat brain. The three-dimensional ESR images of the head of rats and mice were consistent with the fact that MC-PROXYL but not carbamoyl-PROXYL is incorporated into the brain. The ESR-CT images were better for mice than rats. However, the quality of the ESR-CT images was still not satisfactory. Although the resolution and sensitivity of the ESR-CT images were worse than those of the autoradiographic images, the former technique has unique features and advantages; e.g., functional, noninvasive and three-dimensional detection.

Animals↗
PubMed2003

Distributions of ethanol and intubation-related lidocaine in the brain of a trauma patient who was brain dead for about 5 days.

A 48-year-old intoxicated man was admitted to a hospital with an acute subarachnoid hemorrhage from a blow to the head following a drinking session. Lidocaine jelly was used to facilitate intubation during cardiopulmonary resuscitation. While his heart resumed beating, he was classified as brain dead and his heart stopped 114 h after admission. His brain was soft and weighed 1.7 kg at autopsy. A small rupture (0.5 by 0.3 cm) of the left vertebral artery and diffuse subarachnoid hemorrhage were observed. Ethanol was detected only in the cerebrum, cerebellum and clotted blood in the superior sagittal sinus at 0.29, 0.15 and 0.12 mg/g, respectively. Lidocaine was also found in these areas at levels of 28, 24 and 7 ng/g, respectively. Significant amounts of ethanol were present in his brain because blood flow stopped after the injury. Smaller amounts of intubation-related lidocaine were probably distributed to the brain by limited cerebral circulation and remained there after circulation ceased. Toxicological analysis of the brain after death was useful for evaluating his state during treatment.

Anesthetics, Local↗
PubMed2001

Non-invasive assessment of blood-brain barrier (BBB) permeability using a gamma camera to detect 99technetium-gluceptate extravasation in rat brain.

The blood-brain barrier (BBB) is a complex structure of endothelial cells, astroglia, pericytes, and perivascular macrophages enclosed by basal lamina. The BBB regulates the entry of blood-borne molecules and cells into the brain, but it is disrupted in various inflammatory conditions of the central nervous system (CNS). We previously showed that 30 min of immobilization stress increased 99technetium-gluceptate (99Tc) extravasation, measured by a gamma counter, in brain regions containing mast cells, an effect blocked by the mast cell stabilizer disodium cromoglycate [Brain Res. 888 (2001) 117]. Here we report the use of a gamma camera to assess BBB permeability by assessing 99Tc extravasation in the rat brain, during and following acute stress, without having to sacrifice the experimental animals. This method also allows for repeated experimentation on the same animal, since the half-life of 99Tc is only 6 h, and permits testing of potential inhibitors of BBB permeability.

Animals↗
PubMed2004

Brain-computer communication based on the dynamics of brain oscillations.

This chapter presents a review of brain-computer communication based on motor imagery and the dynamics of brain oscillations. The concept of motor imagery as experimental strategy and the two different modes of operation a brain-computer interface can have are explained. An EEG based brain switch that can control a FES-induced hand grasp of a tetraplegic and an approach towards an ECoG based brain switch are presented.

Brain↗
PubMed2001

Multidrug resistance in brain tumors: roles of the blood-brain barrier.

Malignant brain tumors and brain metastases present a formidable clinical challenge against which no significant advances have been made over the last decade. Multidrug resistance (MDR) is one of the main factors in the failure of chemotherapy against central nervous system tumors. The MDR1 gene encoding P-glycoprotein (P-gp), a drug efflux pump which plays a significant role in modulating MDR in a wide variety of human cancers, is highly expressed in the blood-brain barrier (BBB). The BBB controls central nervous system exposure to many endogenous and exogenous substances. The exact molecular mechanisms by which the BBB is involved in the resistance of brain tumors to chemotherapy remain to be identified. The purpose of this review is to summarize reports demonstrating that P-gp, one of the most phenotypically important markers of the BBB, is present in primary brain tumors and thus plays a crucial role in their clinical resistance to chemotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Design and characterization of liposomes containing long-chain N-acylPEs for brain delivery: penetration of liposomes incorporating GM1 into the rat brain.

PURPOSE: To develop a suitable liposomal carrier to encapsulate neu roactive compounds that are stable enough to carry them to the brain across the blood-brain barrier with the appropriate surface characteri tics for an effective targeting and for an active membrane transport. METHODS: Liposomes containing glycosides and a fusogenic lipid were prepared by extrusion. Photon correlation spectroscopy, fluorescent spectroscopy, and differential scanning calorimetry were used to characterize liposomal preparations. Tissue distribution was determined by using 3H-cholesterylhexadecylether as a marker. RESULTS: The incorporation of glycoside determinants and N-palmitoylphosphatidylethanolamine gives liposomes with similar in tial size, trapped volume, negative surface charge, bilayer fluidity, and melting temperature, except for monosialoganglioside-containing liposomes, which showed less negative surface charge and the highe size, trapped volume and melting temperature. All glycosilated formulations gave liposomes able to retain up to the 95% of encapsulated carboxyfluorescein after 90 min at physiologic temperature even in the presence of serum. Monosialoganglioside liposomes were recovered in the cortex, basal ganglia, and mesencephalon of both brain hemispheres. The liver uptake was higher for sulfatide- and glucose-liposomes, whereas the higher blood levels were observed for glucose- and mannose-liposomes. CONCLUSIONS: These results show the suitability of such liposomal formulations to hold encapsulated drugs. Moreover, the brain uptake of monosialoganglioside liposomes makes them good candidates as drug delivery systems to the brain.

Animals↗
PubMed1985

Two-day starvation does not alter the kinetics of blood--brain barrier transport and phosphorylation of glucose in rat brain.

The blood-brain barrier (BBB) transport and brain phosphorylation of glucose were assessed in conscious rats subjected to 2 days of starvation. Although plasma glucose decreased, no significant changes in brain blood flow, BBB glucose transport, or 2-deoxy-D-glucose phosphorylation were observed. The data suggest that adaptive changes of brain glucose metabolism previously observed in starvation are located beyond the initial steps of brain entry and phosphorylation.

Animals↗