Morphological Alterations of the Blood-Brain Barrier in Experimental Serum Sickness (ESS)

1976 ◽  
Vol 34 ◽  
pp. 94-95
Author(s):  
Davis Donald A. ◽  
Milhorat Thomas H.
Keyword(s):  
Blood Brain Barrier ◽  
Serum Sickness ◽  
Brain Barrier ◽  
Periventricular White Matter ◽  
Tissue Samples ◽  
Morphological Alterations ◽  
Cerebral Capillaries ◽  
Blood Brain ◽  
Male Wistar Rats ◽  
The One

Information concerning the effects of systemic diseases on the blood-brain barrier is limited. Lampert and Carpenter (1) and Lampert et al. (2) have shown that experimental lead encephalalopathy produces a toxic vasculitis which permits intravascularly injected thorotrast to escape from cerebral capillaries into the perivascular and extracellular spaces. Other experiments (summarized in 3) have demonstrated an increased permeability of cerebral capillaries as a consequence of cerebral trauma, chemically induced vasculitis, hypertension, and radiation.Acute serum sickness was produced in adult male Wistar rats according to the “one shot” technique of Kniker and Cochrane (4). After seven to eight days the animals were decapitated and tissue samples from the cerebral cortex and periventricular white matter were quickly excised and placed in vials for prefixation in 1% depolymerized paraformaldehyde and 31 purified glutaraldehyde in 0.1M phosphate buffer (pH 7.5) for 24 hours at 4C.

scholarly journals Effects of cadmium on the glial architecture in lizard brain

2017 ◽  
Author(s):  
Rossana Favorito ◽  
Antonio Monaco ◽  
Maria C. Grimaldi ◽  
Ida Ferrandino
Keyword(s):  
Blood Brain Barrier ◽  
Glial Cells ◽  
Toxic Metal ◽  
Chemical Exposure ◽  
Brain Barrier ◽  
Cresyl Violet ◽  
Cytotoxic Action ◽  
Morphological Alterations ◽  
Blood Brain ◽  
The Brain

The glial cells are positioned to be the first cells of the brain parenchyma to face molecules crossing the blood-brain barrier with a relevant neuroprotective role from cytotoxic action of heavy metals on the nervous system. Cadmium is a highly toxic metal and its levels in the environment are increasing due to industrial activities. This element can pass the blood-brain barrier and have neurotoxic activity. For this reason we have studied the effects of cadmium on the glial architecture in the lizard Podarcis siculus, a significant bioindicator of chemical exposure due to its persistence in a variety of habitats. The study was performed on two groups of lizards. The first group of P. siculus was exposed to an acute treatment by a single i.p. injection (2 mg/kg-BW) of CdCl2 and sacrificed after 2, 7 and 16 days. The second one was used as control. The histology of the brain was studied by Hematoxylin/Eosin and Cresyl/Violet stains while the glial structures were analyzed by immunodetection of the glial fibrillary acidic protein (GFAP), the most widely accepted marker for astroglial cells. Evident morphological alterations of the brain were observed at 7 and 16 days from the injection, when we revealed also a decrease of the GFAP-immunopositive structures in particular in the rhombencephalic ventricle, telencephalon and optic tectum. These results show that in the lizards an acute exposure to cadmium provokes morphological cellular alterations in the brain but also a decrement of the expression of GFAP marker with possible consequent damage of glial cells functions.

scholarly journals ALCAM (CD166) is involved in extravasation of monocytes rather than T cells across the blood–brain barrier

2016 ◽  
Vol 37 (8) ◽  
pp. 2894-2909 ◽  
Author(s):  
Ruth Lyck ◽  
Marc-André Lécuyer ◽  
Michael Abadier ◽  
Christof B Wyss ◽  
Christoph Matti ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Th1 Cells ◽  
Human Brain Tissue ◽  
Autoimmune Encephalomyelitis ◽  
Tissue Samples ◽  
Blood Brain ◽  
Static Conditions ◽  
In Vitro Bbb Model

Activated leukocyte cell adhesion molecule (ALCAM) has been proposed to mediate leukocyte migration across the blood–brain barrier (BBB) in multiple sclerosis or experimental autoimmune encephalomyelitis (EAE). Here, we confirmed vascular ALCAM expression in human brain tissue samples in situ and on two different human in vitro BBB models. Antibody-mediated inhibition of ALCAM reduced diapedesis of human CD4+ Th1 but not of Th17 cells across the human BBB in vitro. In accordance to human Th1 cells, mouse Th1 cells showed reduced diapedesis across an ALCAM−/− in vitro BBB model under static but no longer under flow conditions. In contrast to the limited role of ALCAM in T cell extravasation across the BBB, we found a contribution of ALCAM to rolling, adhesion, and diapedesis of human CD14+ monocytes across the human BBB under flow and static conditions. Taken together, our study highlights the potential differences in the CNS expression of ALCAM in mouse and human and supports a prominent role for ALCAM in the multi-step extravasation of monocytes across the BBB.

Abstract 1122‐000167: Hyperintense Acute Reperfusion Marker and Hemorrhagic Conversion in Stroke Patients Undergoing Mechanical Reperfusion

2021 ◽  
Vol 1 (S1) ◽  
Author(s):  
Pouria Moshayedi ◽  
Hamidreza Saber ◽  
David S Liebeskind ◽  
Jeffrey Gornbein ◽  
Bryan Yoo ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
White Matter ◽  
Clinical Outcome ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Periventricular White Matter ◽  
Vessel Occlusion ◽  
Blood Brain ◽  
Ischemic Core ◽  
Core Volume

Introduction : Endovascular thrombectomy (EVT) is a highly effective treatment to improve clinical outcome in patients with acute ischemic stroke due to large vessel occlusion (AIS‐LVO). However, blood‐brain barrier (BBB) disruption causing hemorrhagic transformation and reperfusion injury can potentially negate the beneficial effect of reperfusion. Studying determinants, frequency, and outcomes of the hyperintense acute reperfusion marker (HARM) sign, a biomarker of BBB disruption, would help to identify individual patients at increased risk, as well as developing therapies to prevent BBB breakdown. Methods : In consecutive AIS‐LVO patients with AIS‐LVO who underwent EVT followed by MRI within the next 24 hours, we evaluated frequency, determinants, and outcomes of HARM sign. Results : Among 81 patients meeting study criteria, age was 71.0 (SD 19.7), 58% female, mean NIHSS was 14.5 (SD 6.8), and time from last known well to treatment was 355 min (IQR 206.5 ‐ 664). HARM sign was observed in 64% (52/81) of patients. On multivariate logistic analysis, presence of HARM sign was independently associated with greater periventricular white matter hyperintensity, higher pre‐EVT ischemic core volume, more proximal target vessel occlusion, and achievement of successful reperfusion or better. Hemorrhagic conversion was seen in 31.8% of patients with HARM sign and 26.7% of patients without HARM sign. Multivariate analysis identified higher blood glucose, lower ASPECT, score and greater post‐EVT ischemic core volume as independent predictors of hemorrhagic conversion. HARM sign was identified to correlate with poor clinical outcome in bivariate analysis, but multivariate analysis only identified less neurological deficits, lower baseline systolic BP, lower degree of periventricular white matter hyperintensities, shorter time to device deployment and reduced post EVT ischemic core volume as independent predictors of good clinical outcome (mRS 0–2) upon discharge. Conclusions : The HARM sign indicating disruption of the blood‐brain barrier following EVT is common, present in about 6 of every 10 treated patients. Independent risk factors for HARM sign are chronic ischemic microangiopathy, greater acute ischemic core, and successful reperfusion. HARM sign presence is associated with worse functional outcome.

scholarly journals Permeability of the blood-brain barrier for sodium iodide in some organic diseases of the nervous system

1937 ◽  
Vol 33 (11) ◽  
pp. 1319-1331
Author(s):  
N. I. Popov
Keyword(s):  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Sodium Iodide ◽  
The Other ◽  
Brain Barrier ◽  
Theoretical Interest ◽  
Blood Brain ◽  
Medicinal Substances ◽  
The One

In the physiology and pathology of the nervous system, much attention is paid to the issue of the permeability of the blood-brain barrier. Along with the theoretical interest, this question is important for the practicing physician. If, on the one hand, a violation of the barrier leads to a disease of the nervous system, then, on the other hand, in diseases of the nervous system, it is often necessary to force the permeability of the barrier in one way or another in order to enable various medicinal substances (arsenic, mercury) to enter the cerebrospinal fluid

scholarly journals LIPID NANOPARTICLES FOR THE TRANSPORT OF DRUGS LIKE DOPAMINE THROUGH THE BLOOD–BRAIN BARRIER

2020 ◽  
Author(s):  
Elena Ortega ◽  
Santos Blanco ◽  
Adolfina Ruiz ◽  
María Ángeles Peinado ◽  
Sebastian Peralta ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Lipid Nanoparticles ◽  
Brain Parenchyma ◽  
Brain Barrier ◽  
Great Stability ◽  
Efficient Treatment ◽  
Blood Brain ◽  
Penetration Ability ◽  
Male Wistar Rats ◽  
The Brain

Diseases and disorders of the nervous system, like Parkinson disease (PD) and others neurodegenerative pathologies are widespread in our society. The arsenal of treatments against these pathologies continues to increase, but in many cases its use is limited. This is due to the blood-brain barrier (BBB), which acts by limiting the penetration of drugs into the brain. To overcome this handicap, in the current research solid lipid nanoparticles (SLNPs) able to encapsulate drugs and to cross the blood-brain barrier have been designed to transport and release these drugs into their targets. These SLNPs were synthesized by a sonication method and high agitation process searching the most adequate physicochemical profile to achieve the objectives set. Today, the most efficient treatment for PD consists of providing the dopamine (DP) that is lost by neurodegeneration; however, the nature of this neurotransmitter prevents its crossing of the BBB. Therefore, DP may be considered as a good candidate to be encapsulated in SLNPs while studying how the loading drug could affect such nanoparticles. Based on these antecedents, in this research, both empty and DP-charged SLNPs were characterized physicochemically. The results obtained indicated a great stability of the nanoparticles loaded with DP when drug was used at 0.2 to 0.05%; these concentrations barely affected its size, polydispersity and ζ-potential, and the SLNPs elaborated in this research were high appropriate to be injected systemically. Finally, empty SLNPs labeled and administered systemically to adult male Wistar rats demonstrate their penetration ability into the brain parenchyma.

On the transfer of visdout to the cerebrospinal fluid in the treatment of syphilis in connection with the doctrine of the blood-brain barrier

1930 ◽  
Vol 26 (7) ◽  
pp. 114-118
Author(s):  
G. G. Kondratyev
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Nervous Tissue ◽  
Joint Venture ◽  
The Other ◽  
Brain Barrier ◽  
Special Mechanism ◽  
Blood Brain ◽  
Harmful Substances ◽  
The One

On the basis of numerous studies, it has been established that some substances introduced into the blood are easily detected in the cerebrospinal fluid and nervous tissue, while others circulating in the blood, even in very significant quantities, do not appear in them under normal conditions. On the contrary, all substances introduced into the joint venture. m., very quickly appear in the blood. This circumstance indicates that between the blood on the one hand, cn. m. f. and nervous tissue on the other hand, apparently, there is a special mechanism of a protective nature, which is able to make a choice between the substances circulating in the blood, selectively passing some and delaying others, and also quickly removing all harmful substances from the joint venture. m f., the so-called. blood-brain barrier (Stern, Gautier).

scholarly journals Age-associated physiological and pathological changes at the blood–brain barrier: A review

2016 ◽  
Vol 37 (1) ◽  
pp. 4-24 ◽  
Author(s):  
Franciska Erdő ◽  
László Denes ◽  
Elizabeth de Lange
Keyword(s):  
Blood Brain Barrier ◽  
Neurodegenerative Disorders ◽  
Neurovascular Unit ◽  
Developed Countries ◽  
Brain Barrier ◽  
Aging Brain ◽  
Pharmacoresistant Epilepsy ◽  
Morphological Alterations ◽  
Blood Brain ◽  
Junction Proteins

The age-associated decline of the neurological and cognitive functions becomes more and more serious challenge for the developed countries with the increasing number of aged populations. The morphological and biochemical changes in the aging brain are the subjects of many extended research projects worldwide for a long time. However, the crucial role of the blood–brain barrier (BBB) impairment and disruption in the pathological processes in age-associated neurodegenerative disorders received special attention just for a few years. This article gives an overview on the major elements of the blood–brain barrier and its supporting mechanisms and also on their alterations during development, physiological aging process and age-associated neurodegenerative disorders (Alzheimer's disease, multiple sclerosis, Parkinson's disease, pharmacoresistant epilepsy). Besides the morphological alterations of the cellular elements (endothelial cells, astrocytes, pericytes, microglia, neuronal elements) of the BBB and neurovascular unit, the changes of the barrier at molecular level (tight junction proteins, adheres junction proteins, membrane transporters, basal lamina, extracellular matrix) are also summarized. The recognition of new players and initiators of the process of neurodegeneration at the level of the BBB may offer new avenues for novel therapeutic approaches for the treatment of numerous chronic neurodegenerative disorders currently without effective medication.

scholarly journals Deoxycholic Acid as a Modifier of the Permeation of Gliclazide through the Blood Brain Barrier of a Rat

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Mladena Lalić-Popović ◽  
Velibor Vasović ◽  
Boris Milijašević ◽  
Svetlana Goločorbin-Kon ◽  
Hani Al-Salami ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Deoxycholic Acid ◽  
Brain Barrier ◽  
Brain Cells ◽  
Diabetic Patients ◽  
Acid Pretreatment ◽  
Blood Brain ◽  
Male Wistar Rats ◽  
Poor Nutrition

Major problem for diabetic patients represents damage of blood vessels and the oxidative stress of the brain cells due to increased concentration of free radicals and poor nutrition of brain cells. Gliclazide has antioxidative properties and poor blood brain barrier (BBB) penetration. Bile acids are known for their hypoglycemic effect and as promoters of drug penetration across biological membranes. Accordingly, the aim of this study is to investigate whether the bile acid (deoxycholic acid) can change the permeation of gliclazide, through the blood brain barrier of a rat model type-1 diabetes. Twenty-four male Wistar rats were randomly allocated to four groups, of which, two were given alloxan intraperitoneally (100 mg/kg) to induce diabetes. One diabetic group and one healthy group were given a bolus gliclazide intra-arterially (20 mg/kg), while the other two groups apart from gliclazide got deoxycholic acid (4 mg/kg) subcutaneously. Blood samples were collected 30, 60, 150, and 240 seconds after dose, brain tissues were immediately excised and blood glucose and gliclazide concentrations were measured. Penetration of gliclazide in groups without deoxycholic acid pretreatment was increased in diabetic animals compared to healthy animals. Also in both, the healthy and diabetic animals, deoxycholic acid increased the permeation of gliclazide through that in BBB.

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