Qualitative Evaluation of the Blood-Brain Barrier after the Use of Hypertonic Saline Solution in Young Rats

2001 ◽  
Vol 33 (5-6) ◽  
pp. 311-317 ◽  
Author(s):  
R.M. Carrera ◽  
A.M. Pacheco Jr. ◽  
R.A. Mastroti
Keyword(s):  
Hypertonic Saline ◽  
Blood Brain Barrier ◽  
Saline Solution ◽  
Qualitative Evaluation ◽  
Brain Barrier ◽  
Hypertonic Saline Solution ◽  
Young Rats ◽  
Blood Brain

Similar effects of hypertonic saline and mannitol on the inflammation of the blood-brain barrier microcirculation after brain injury in a mouse model

2012 ◽  
Vol 73 (2) ◽  
pp. 351-357 ◽  
Author(s):  
Joshua A. Marks ◽  
Shenghui Li ◽  
Wanfeng Gong ◽  
Paymon Sanati ◽  
Rachel Eisenstadt ◽  
...  
Keyword(s):  
Brain Injury ◽  
Mouse Model ◽  
Hypertonic Saline ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

Paroxysmal slow cortical activity in Alzheimer’s disease and epilepsy is associated with blood-brain barrier dysfunction

2019 ◽  
Vol 11 (521) ◽  
pp. eaaw8954 ◽  
Author(s):  
Dan Z. Milikovsky ◽  
Jonathan Ofer ◽  
Vladimir V. Senatorov ◽  
Aaron R. Friedman ◽  
Ofer Prager ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Causative Role ◽  
Barrier Dysfunction ◽  
Therapeutic Implications ◽  
Young Rats ◽  
Blood Brain ◽  
Nonconvulsive Seizures

A growing body of evidence shows that epileptic activity is frequent but often undiagnosed in patients with Alzheimer’s disease (AD) and has major therapeutic implications. Here, we analyzed electroencephalogram (EEG) data from patients with AD and found an EEG signature of transient slowing of the cortical network that we termed paroxysmal slow wave events (PSWEs). The occurrence per minute of the PSWEs was correlated with level of cognitive impairment. Interictal (between seizures) PSWEs were also found in patients with epilepsy, localized to cortical regions displaying blood-brain barrier (BBB) dysfunction, and in three rodent models with BBB pathology: aged mice, young 5x familial AD model, and status epilepticus–induced epilepsy in young rats. To investigate the potential causative role of BBB dysfunction in network modifications underlying PSWEs, we infused the serum protein albumin directly into the cerebral ventricles of naïve young rats. Infusion of albumin, but not artificial cerebrospinal fluid control, resulted in high incidence of PSWEs. Our results identify PSWEs as an EEG manifestation of nonconvulsive seizures in patients with AD and suggest BBB pathology as an underlying mechanism and as a promising therapeutic target.

Lack of effects of 1439 MHz electromagnetic near field exposure on the blood-brain barrier in immature and young rats

2005 ◽  
Vol 26 (7) ◽  
pp. 578-588 ◽  
Author(s):  
Masanori Kuribayashi ◽  
Jianqing Wang ◽  
Osamu Fujiwara ◽  
Yuko Doi ◽  
Kyoko Nabae ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Near Field ◽  
Brain Barrier ◽  
Field Exposure ◽  
Young Rats ◽  
Blood Brain

Influence d'un retard de croissance sur la perméabilité de la barrière hémato-encéphalique chez le rat nouveau-né exposé au plomb

1984 ◽  
Vol 62 (1) ◽  
pp. 142-145 ◽  
Author(s):  
John Turnbull ◽  
Jules Brodeur
Keyword(s):  
Blood Brain Barrier ◽  
Growth Retardation ◽  
Trypan Blue ◽  
Normal Diet ◽  
Brain Barrier ◽  
Free Access ◽  
Postnatal Maturation ◽  
Young Rats ◽  
Nutritional Effect ◽  
Blood Brain

Postnatal administration of lead to young rats via maternal milk increases the permeability of the blood–brain barrier to trypan blue. However, since this regimen delays postnatal maturation, the question arises whether growth retardation per se could explain the altered permeability to the dye. The present investigation was undertaken to examine this possibility. A first group of newborn rats were fed by dams having free access to normal food; a second group was fed by dams receiving 3% lead as the acetate salt in their food; a third group was fed by dams whose normal diet was restricted to the amount taken daily by dams of the second group. Signs of encephalopathy as shown by urinary incompetence and hind-limb paralysis were observed only in young pups exposed to lead; similarly, only the latter showed increased brain permeability to trypan blue. These results suggest that the altered permeability of the blood–brain barrier in young rats is the direct consequence of lead toxicity and not of growth retardation secondary to a nutritional effect of lead.

The mechanism of opening of the blood-brain barrier by hypertonic saline

1985 ◽  
Vol 24 (9) ◽  
pp. 909-913 ◽  
Author(s):  
A GULATI ◽  
S AGARWAL ◽  
R SHUKLA ◽  
R SRIMAL ◽  
B DHAWAN
Keyword(s):  
Hypertonic Saline ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Blood-brain barrier breakdown and repair following gliotoxic drug injection in the brainstem of streptozotocin-diabetic rats

2012 ◽  
Vol 70 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Eduardo Fernandes Bondan ◽  
Maria de Fátima Monteiro Martins
Keyword(s):  
Blood Brain Barrier ◽  
Saline Solution ◽  
Diabetic Rats ◽  
Brain Barrier ◽  
Intravenous Route ◽  
Carbon Particles ◽  
Blood Brain ◽  
Streptozotocin Diabetic Rats ◽  
Barrier Breakdown ◽  
Blood Brain Barrier Breakdown

Ethidium bromide (EB) causes local astrocytic disappearance, with glia limitans disruption and blood-brain barrier (BBB) breakdown. The aim of this study was to evaluate the BBB integrity after the injection of 0.1% EB or 0.9% saline solution into the cisterna pontis of Wistar rats submitted or not to the streptozotocin diabetogenic model. Brainstem sections were collected from 24 hours to 31 days post-injection for ultrastructural analysis and glial fibrillary acidic protein immunohistochemical staining. Some animals received colloidal carbon ink by intravenous route at the same periods. In rats injected with EB, results revealed astrocyte disappearance and leakage of carbon particles beginning at 48 hours and persisting for 7 days in non-diabetic rats and for 15 days in the diabetic ones, although, in both groups, several areas remained devoid of astrocytic processes up to 31 days. In rats injected with saline, there was no sign of astrocytic loss or carbon particles leakage.

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