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At least 19 recordsLinked to original sources

PubMed1984

Osmotic blood-brain barrier modification and combination chemotherapy: concurrent tumor regression in areas of barrier opening and progression in brain regions distant to barrier opening.

Chemotherapeutic drug delivery can be enhanced by administering drugs into the internal carotid or vertebral artery circulation after osmotic opening of the blood-brain barrier (BBB). As evidence of the clinical implications of this technique, radiographic documentation of central nervous system (CNS) tumor regression was observed in three patients concurrent with the development of new tumor nodule(s) in portions of the brain distant from the region of osmotic blood-brain barrier opening. These three patients, one with metastatic carcinoma of the breast, one with glioblastoma, and one with primary CNS lymphoma, highlight the importance of drug delivery to CNS malignancies.

Adult↗

PubMed1987

Membranes and barriers: with a focus on the gastric mucosal barrier.

In this review I have discussed the importance of barriers retarding the transport of electrolytes, non-electrolytes, proteins, and water to the maintenance of physiological homeostasis, and how disruption of these barriers can lead to severe pathological consequences. At the cellular level, I have discussed the potential localization of these barriers to molecular diffusion as being at the intercellular junction, plasmalemmal membrane, and at the extracellular surface of the plasma membrane. The presence of barriers in the major organ systems of the body is noted and these are listed, together with the physiological need for their restrictive-permeability properties. Emphasis is then placed on 2 of these barriers, the blood-brain barrier and the gastric mucosal barrier, and common characteristics of these systems are discussed. I have outlined our present knowledge of the molecular basis of the gastric mucosal barrier and, specifically, the contribution of the surface barrier constituents: mucus, bicarbonate, and surface-active lipids (glycolipids and phospholipids). Lastly, I have discussed our recent experiments pertaining to the possible importance of a hydrophobic water-repellent lining to the stomach's resistance to luminal acid.

Animals↗

PubMed1991

Sphingolipids are required for mammalian epidermal barrier function. Inhibition of sphingolipid synthesis delays barrier recovery after acute perturbation.

Stratum corneum lipids comprise an approximately equimolar mixture of sphingolipids, cholesterol, and free fatty acids, arranged as intercellular membrane bilayers that are presumed to mediate the epidermal permeability barrier. Prior studies have shown that alterations in epidermal barrier function lead to a rapid increase in cholesterol and fatty acid synthesis which parallels the early stages of the repair process. Despite an abundance of indirect evidence for their role in the barrier, the importance of sphingolipids has yet to be demonstrated directly. Whereas sphingolipid synthesis also increases during barrier repair, this response is delayed in comparison to cholesterol and fatty acid synthesis (Holleran, W.M., et al. 1991. J. Lipid Res. 32:1151-1158). To further delineate the role of sphingolipids in barrier homeostasis, we assessed the impact of inhibition of sphingolipid synthesis on epidermal barrier recovery. A single topical application of beta-chloro-L-alanine (beta-CA), an irreversible inhibitor of serine-palmitoyl transferase (SPT), applied to acetone-treated skin of hairless mice resulted in: (a) greater than 75% inhibition of SPT activity at 30 min (P less than 0.001); (b) a global decrease in sphingolipid synthesis between 1 and 3 h (P less than 0.02); (c) reduction of epidermal sphingolipid content at 18 h (P less than 0.01); (d) delayed reaccumulation of histochemical staining for sphingolipids in the stratum corneum; and (e) reduced numbers and contents of lamellar bodies in the stratum granulosum. Finally, despite its immediate, marked diminution of sphingolipid synthesis, beta-CA slowed barrier recovery only at late time points (greater than 6 h) after acetone treatment. This inhibition was overridden by coapplications of ceramides (the distal SPT product), indicating that the delay in repair was not due to non-specific toxicity. These studies demonstrate a distinctive role for epidermal sphingolipids in permeability barrier homeostasis.

Acyltransferases↗

PubMed1984

Ultrastructural and histophysiological studies on the blood-nerve barrier and perineurial barrier in leprosy neuropathy.

Onset and nature of ultrastructural changes in endoneurial vasa nervorum during the pathogenesis of leprosy neuropathy and possibly associated alterations in the "blood-nerve barrier" were investigated, together with perineurial barrier functioning, in mice infected 20-28 months previously with Mycobacterium leprae and in (ageing) non-infected mice. Barriers were tested by i.v. administration of markers (Trypan blue and ferritin) 1-4 days before killing the mice. Twenty-eight months after infection, histopathology of sciatic nerves was comparable to that seen in sensory nerves in clinically early human (borderline-) lepromatous leprosy. Schwann cells and endoneurial macrophages were bacillated, endothelia of endoneurial vessels not, and the perineurium rarely. Many infected mice and all (ageing) controls possessed ultrastructurally and functionally normal endoneurial vessels. Their continuous endothelium with close junctions had prevented marker passage, even when surrounding endoneurial tissue cells were quite heavily bacillated. The perineurium was also normal. By contrast, in infected mice showing hind limb paralysis serious histopathologic involvement and large globi of bacilli intrafascicularly in sciatic nerves, endoneurial blood vessels were abnormal. Open endothelial junctions, extreme attenuation, fenestrations, and luminal protrusions were all features comparable to neural microangiopathy encountered in leprosy patients (Boddingius 1977a, b). The "blood-nerve barrier" clearly had become defective allowing excessive exudation of Trypan blue and ferritin, via four pathways from the vessel lumen, deep into surrounding endoneurial tissues but halted by a normal perineurial barrier. Markers in such "blue" nerves were not found in bacillated or non-bacillated Schwann cells, thus denying significant phagocytotic and lysosomal activities of Schwann cells at this stage of neuropathy. Possible implications of barrier performances for anti-leprosy drug treatment of patients are discussed.

Age Factors↗

PubMed1982

Effects of adrenal cortical steroids and osmotic blood-brain barrier opening on methotrexate delivery to gliomas in the rodent: the factor of the blood-brain barrier.

The effect of adrenal cortical steroids and osmotic blood-brain barrier modification on methotrexate delivery to normal and glioma-bearing rats was studied. In animals with the avian sarcoma virus-induced glioma, osmotic blood-brain barrier modification resulted in significantly increased delivery of methotrexate to the tumor-bearing hemisphere (including the tumor, the brain around the tumor, and the brain distant to the tumor), compared to the nonmodified hemisphere or to control animals. The administration of adrenal steroids, followed by intracarotid methotrexate, resulted in slightly decreased chemotherapeutic agent (methotrexate) delivery to the tumor, the brain around the tumor, and the brain distant to the tumor. When adrenal steroids were given prior to barrier modification and methotrexate therapy, the level of methotrexate was significantly less in the tumor. These studies provide evidence that the blood-brain barrier exists in tumors and is a factor in drug delivery to tumors. Steroid administration greatly interferes with the enhancement of drug delivery to tumors that can be achieved with osmotic blood-brain barrier modification.

Alpharetrovirus↗

PubMedDate not supplied

Topographical distribution of barrier function in cervico-cephalic arteries of dog. Major cerebral arteries possess definite barrier function?

Topographic distribution of barrier function in normal canine cervico-cephalic arteries was studied using horseradish peroxidase (HRP) and Evans blue as tracers. The carotid sinus of the internal carotid artery (ICA) was conspicuously permeable to HRP when compared to other areas of major cervical arteries. The cavernous portion of the ICA also showed prominent permeation of HRP, especially through the outer surface, which is covered with venous endothelial cells. On the luminal side of the cavernous portion of the ICA, barrier deficiency was noted at angulated segments such as the carotid siphon. Intracranial segments of both ICA and vertebral arteries demonstrated incomplete barrier function of the first 1 to 4 mm from the origin of the intradural segments. These areas were considered to be transitional sites in barrier function between extra- and intracranial arteries. Focal, but definite, barrier disruption was also noted at the distal ends of the ICA and other arterial branching sites of major intracranial arteries. While opening of the interendothelial junctions was considered to be one of the mechanisms causing increased permeability in the cavernous ICA, the mechanisms for the permeation of HRP into the major cerebral arteries could not be confirmed ultrastructurally.

Animals↗

PubMedDate not supplied

The effect of toxic doses of lanthanum and cerium on the placental barrier and the blood/organ barrier in mice after intravenous injection of these elements.

In earlier studies the toxicity of the lanthanides was determined on the basis of the LD50/30 value, increase of serum ornithine carbamoyltransferase activity, and the degree of passage of the lanthanides to the fetuses and milk. The purpose of the present work was to investigate the effects of toxic doses of lanthanum and cerium on the function of the placental barrier and the blood/organ barrier in mice using substances of known molecular weight labelled with radionuclides (14C-aminoisobutyric acid--AIB, 3H-thymidine and 125I-albumin). Increased uptake of 14C-AIB and 3H-thymidine was demonstrated in the liver, spleen and placenta of mice after toxic doses of La and Ce indicating disturbances in the function of the blood/organ barrier (liver, spleen, placenta) due to damage to the vascular endothelium or cell membranes. No disturbances were shown in the function of the placental barrier (which would have caused increased passage of these markers to the fetus), and rupture of the cell membranes in the studied tissues was not demonstrated (it would have caused increased passage of 125I-albumin, a macromolecular compound) in any of the studied organs in mice.

Animals↗

PubMed1991

Blood-nerve barrier in the frog during wallerian degeneration: are axons necessary for maintenance of barrier function?

Blood-nerve barrier tissues (endoneurial blood vessels and perineurium) of the frog's sciatic nerve were studied during chronic Wallerian degeneration to determine whether barrier function depends on the presence of intact axons. Sciatic nerves of adult frogs were transected in the abdominal cavity; the ends were tied to prevent regeneration and the distal nerve stumps were examined. Vascular permeabilities to horseradish peroxidase and to [14C]sucrose increased to day 14, returned toward normal levels by 6 weeks, and continued at near normal levels to 9 months. Perineurial permeabilities to the tracers increased by day 10 and remained elevated at 9 months. Proliferation of perineurial, endothelial, and mast cells occurred between 3 days and 6 weeks, resulting in an increased vascular space (measured with [3H]dextran) and number of vascular profiles. The perineurium increased in thickness and the mast cells increased in number. This study indicates that during Wallerian degeneration of the frog's sciatic nerve there is 1) a transitory increase in vascular permeability distal to the lesion, that is related to changes within the endoneurium; 2) an irreversible increase in permeability of the perineurium, which begins later than that seen in the endoneurial blood vessels; and 3) proliferation of non-neuronal components in the absence of regenerating neuronal elements. The results indicate that maintenance of vascular integrity does not require the presence of axons in the frog's peripheral nerve, whereas perineurial integrity and barrier function are affected irreversibly by Wallerian degeneration.

Animals↗

PubMed1992

New condoms for men and women, diaphragms, cervical caps, and spermicides: overcoming barriers to barriers and spermicides.

Barriers and spermicides are being developed for the prevention of unwanted pregnancy and sexually transmitted infection. The inconvenience of current methods limits their acceptability and leads to higher user failure rates. New methods, such as female condoms, nonlatex male condoms, and new cervical caps are being developed: the Reality (Wisconsin Pharmacal, Jackson, WI) polyurethane vaginal pouch has already received conditional Food and Drug Administration approval for use in the United States. The material used in a Food and Drug Administration-approved nonallergenic glove is being tested for its effectiveness as a condom. In addition, the Fem Cap, a cervical cap that had a life table probability of failure within 1 year of 4.8%, is expected to be available within the next 2 years. It is important for clinicians to be informed of new options becoming available for those patients who may be good candidates for these barrier methods.

Contraceptive Devices↗

PubMed1985

The mouse blood-brain barrier and blood-nerve barrier for IgG: a tracer study by use of the avidin-biotin system.

To study the permeability of the blood-brain barrier (BBB) and the blood-nerve barrier (BNB) for immunoglobulin G (IgG) we adapted the avidin-biotin system for postembedding demonstration of the tracer IgG in the central and peripheral nervous system (CNS, PNS). Normal mouse and human IgG were biotinylated and injected daily into the intraperitoneal (i.p.) space of adult BDF1 mice. After 24h, IgG was detected in blood vessels and in the interstitium of various organs, but staining was restricted to the dura mater in the CNS, to the spinal ganglia, and to the perineurium of peripheral nerves. After 4 days, IgG was also present in the endoneurial connective tissue of peripheral nerves, while the brain, spinal cord, and spinal roots remained free of IgG. Our results show a partial permeability of the normal mouse BNB for homologous and heterologous IgG.

Animals↗

PubMed1992

HT7, Neurothelin, Basigin, gp42 and OX-47--many names for one developmentally regulated immuno-globulin-like surface glycoprotein on blood-brain barrier endothelium, epithelial tissue barriers and neurons.

The antigens HT7 and Neurothelin were recently described as inducible membrane glycoproteins on chick blood-brain barrier endothelium. Our results demonstrate that the Neurothelin antibody 1W5 does recognize the isolated HT7 protein as well as the HT7 protein expressed by COS-1 cells transfected with the HT7 cDNA. Therefore, the HT7 and Neurothelin epitopes can be found on an unique glycoprotein. By low stringency hybridization we have isolated the murine cDNA clone encoding the homologous murine protein. The nucleotide sequence of the open reading frame is identical to that of the cDNA clones encoding the gp42 protein and the Basigin antigen expressed in F9 cells and in the early mouse embryo. The murine amino acid sequence shows 94% identity with the rat OX-47 membrane glycoprotein which was shown to be expressed in blood-brain barrier endothelium and several epithelial cell layers. These results demonstrate that HT7, Neurothelin, gp42, Basigin and OX-47 are different names for probably the same glycoprotein in different species.

Amino Acid Sequence↗

PubMed1991

[Ultrastructure of the cerebrospinal fluid-brain barrier of the cerebral ventricles and blood-brain barrier of the vascular plexus in experimental aseptic leptomeningitis].

The CSF-encephalic barrier of brain ventricles was examined at the submicroscopic level at different times of experimental aseptic leptomeningitis. In the acute period of the pathology, (3 to 7 days) the integrity of the bar was found to be disturbed because of acute inflammatory phenomena. In the subacute period (15 to 30 days), CSF hypertension was demonstrable. In the chronic period (90 days), the development of dystrophic and degenerative processes in the structures of the ependyma and vascular plexus were related to the disorders in CSF- and hemodynamics of the brain. Occlusion of the CSF tract was found to be associated with the impairment of the integrity of the blood- and CSF-encephalic barriers, marked edema end disintegration of the nerve tissue.

Acute Disease↗

PubMed1986

Expression of mouse beta 2-microglobulin in frozen and formaldehyde-fixed central nervous tissues: comparison of tissue behind the blood-brain barrier and tissue in a barrier-free region.

Previous work indicates that the weak expression in neural tissues of beta 2-microglobulin (beta 2-m) and major histocompatibility complex (MHC) class I gene products can be increased experimentally. Physiologic conditions in which greater neural MHC expression occurs are not well defined. Here we have asked whether protection from blood-borne antigens afforded by the blood-brain barrier is related to the lack of MHC expression. A rabbit antiserum raised against purified mouse beta 2-m was used in an immunocytochemical assay. The serum reacted strongly with lymphoid tissues and was inhibited by purified beta 2-m. No beta 2-m was detected in neurons or glia in any brain area examined. A barrier-free region, the area postrema, showed the same lack of neural cell staining. Blood vessel walls in the same sections were beta 2-m+. It is unlikely that these staining patterns are due to cell type-specific beta 2-m degradation, since frozen and formaldehyde-perfused, paraffin-embedded preparations gave similar results. Failure to detect beta 2-m in the area postrema suggests that passive exposure to environmental antigens, immunomodulators, or immunocompetent cells is not sufficient to induce neural class I expression. Rather, if increased expression of beta 2-m and class I occurs in vivo, additional stimulus is required.

Animals↗

PubMed1984

Correlations between changes in indicators of gastric mucosal barrier integrity at time of exposure to "barrier breakers" and extent of hemorrhagic erosions one hour later.

We have examined the effects of seven different "barrier breakers" (including ethanol, aspirin, salicylic acid, isobutyric acid, Na taurocholate, thermal injury, and hyperosmotic glucose) on chambered gastric mucosae of rats in an attempt to identify variations in accepted indicators of mucosal barrier integrity which would accurately predict the extent of subsequent hemorrhagic erosion. When results from all experimental groups were considered, only the initial decrease in transmucosal potential difference (PD) showed significant correlation with final damage (lesion area). When the results were analyzed as separate subgroups, significant correlations were also found between net K+ efflux during the first 10 min after luminal infusion and final lesion area. Only in the subgroup containing ethanol, salicylates, and thermal injury was there a correlation between net loss of luminal H+ (back-diffusion) and lesion area. These results are considered in terms of their implications for the ulcerogenic actions of each group of agents.

Animals↗

PubMed1990

Cognitive and motor deficits in the performance of an object retrieval task with a barrier-detour in monkeys (Cercopithecus aethiops sabaeus) treated with MPTP: long-term performance and effect of transparency of the barrier.

To assess the stability of neural deficits produced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the performance of monkeys on an object retrieval (detour) task was studied. The task required retrieval of a banana slice from a transparent box open on one side and fastened to a tray in front of the cage. The orientation of the open side, position on the tray, and position of the banana in the box were manipulated to vary the difficulty of the trials. Six African green monkeys (Cercopithecus aethiops sabaeus) were treated with MPTP (1.5-1.6 mg/kg cumulative doses over 4-5 days) and compared with 5 saline-treated control monkeys. The MPTP-treated monkeys had no gross neurological deficits but did have motor and cognitive deficits during acquisition of the object retrieval task 8-12 months after treatment (J. R. Taylor, Elsworth, Roth, Sladek, & Redmond, in press). Performance on the task was examined for 3 months after it had been learned. The MPTP-treated subjects reached at the barrier (transparent side) significantly more than controls and were less successful at retrieving the reward on the 1st reach than controls. Although they took longer to initiate the reach and had more motor problems than controls, they were as likely as controls to retrieve the reward in the end. These deficits remained stable throughout testing. An opaque but otherwise identical box was used randomly on some trials. MPTP-treated subjects decreased barrier reaches to control levels on trials in which the opaque box was used, whereas motor problems increased compared with trials in which the transparent box was used. The task can detect subtle performance deficits similar to those found in Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1984

Effect of 2450 MHz microwave energy on the blood-brain barrier to hydrophilic molecules. D. Brain temperature and blood-brain barrier permeability to hydrophilic tracers.

Measurement of temperature within the cerebral cortex, hypothalamus, cerebellum and medulla of rats sham-, heat- or microwave-exposed revealed the presence of a thermal gradient within the brain. In all groups, cerebral cortex and the cerebellum were cooler than the deeper hypothalamus and medulla. Exposure to 2450 MHz CW microwaves or ambient heat (42 +/- 2 degrees C) resulted in measurable elevation of regional brain temperature, but without alteration of temperature gradients normally observed within the brain. Exposure to 20 mW/cm2 (SAR approximately equal to 4 W/kg) for 30, 90 or 180 min induced a small, but significantly (U = 0, P less than 0.05) increased temperature of the colon, and in each region of the brain studied. Exposure to an incident power density of 65 mW/cm2 (SAR approximately equal to 13.0 W/kg) for 30 or 90 min or to ambient heat (42 +/- 2 degrees C) for 90 min resulted in a substantially greater thermal response as indicated by higher colonic and brain temperatures. Comparison of regional brain temperature with individual colonic temperatures is expressed as delta T = t degrees Cbrain--t degrees Ccolon. In general delta T values for ambient heat or microwave-exposed rats did not differ significantly from those of sham-exposed animals. Exposure to microwaves or ambient heat did not alter the general relationships between regional brain and colonic temperatures, i.e., cortical and cerebellar temperatures were always below and hypothalamic and medullary temperatures always above corresponding colonic temperatures. The plotted temperature data (brain vs colonic temperature) indicate a linear relationship between brain and colonic temperatures. Levels of sodium fluorescein (NAFl), horseradish peroxidase (HRP) and [14C]sucrose (described in preceding papers) within the brain show a high correlation (P less than 0.05) with brain temperature. Suppression of blood-brain barrier permeability to hydrophilic tracers was most pronounced at brain temperatures exceeding approximately 40 degrees C and is demonstrated to be temperature dependent.

Animals↗

PubMed1992

Gastric mucosal barrier: barrier to hydrogen ions imparted by gastric surfactant in vitro.

A simple experiment is described which shows how the highly surface active ingredient of gastric surfactant (DPPC) can be deposited on a filter paper to reduce the rate of transmission of hydrogen ions by one to two orders of magnitude. This finding is compatible with previous studies implying that the hydrophobic layer of surface active phospholipid provides the gastric mucosal barrier as a distinct physical entity.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1983

The anionic barrier of blood vessel walls and the possible pathologic changes due to the deionization of the barrier and plasma proteins.

For the purpose to observe the possible vessel wall damage by deionization of the related anionic groups the perfusion test of rat kidney and aorta with cationic iron colloid particles and the injection experiments with albumin-poly-L-lysine complex were carried out. By staining the fixed tissue sections with the cationic iron colloid at pH 7.3 the ionized anionic sites on vessel walls have been demonstrated histochemically. The perfusion test of living tissue with the cationic iron colloid induced the desquamation of the endothelial cells. The perfused colloid particles were adsorbed to the whole endothelial cell surfaces facing to luminal and subluminal sides. Albumin-poly-L-lysine complex injected into vein deposited in the subendothelial spaces of glomerular capillaries through the endothelial cell layer having the well-kept anionic barriers. Discussion was made on possible damage of vessels due to the deionization of anionic groups of endothelial cells and serum proteins by general cationic molecules.

Adsorption↗