scholarly journals New cerebrovascular agent with hypotensive activity

2019 ◽  
Vol 5 (2) ◽  
pp. 71-77
Author(s):  
Galina A. Kim ◽  
Tamara S. Gan’shina ◽  
Elena V. Kurza ◽  
Ilya N. Kurdyumov ◽  
Denis V. Maslennikov ◽  
...  
Keyword(s):  
Blood Flow ◽  
Antihypertensive Agent ◽  
Brain Injuries ◽  
Cerebrovascular Disorders ◽  
Male Rats ◽  
Hypotensive Activity ◽  
Duration Of Action ◽  
Ischemic Brain ◽  
Cerebrovascular Activity ◽  
The Brain

Introduction: In cerebrovascular disorders, special attention is paid to a hypertensive cerebrovascular crisis, which combines a vascular injury of the brain and hypertension. The paper studies the cerebrovascular properties of the calcium channel blocker of S-Amlodipine nicotinate antihypertensive agent. Materials and methods: Tests were performed on 96 nonlinear male rats, measuring local blood flow in the cerebral cortex in 36 awake animals, using a laser Doppler flowmeter. Cerebral circulation was recorded in the animals when modeling ischemic and hemorrhagic brain injuries. Results and discussion: S-Amlodipine nicotinate (0.1 mg/kg i/v) shows a pronounced cerebrovascular activity in the models of ischemic and hemorrhagic injuries of the brain. In terms of the vasodilating effect in ischemic brain injury, the drug is comparable to mexidol, nimodipine, picamilon, but is superior to nimodipine and picamilon in terms of duration of action, and in the model of hemorrhagic stroke, S-Amlodipine nicotinate is superior to nimodipine and is comparable to picamilon and mexidol. The analysis of the mechanism of action of the agent revealed the participation of GABA A-receptors in the implementation of cerebrovascular properties of the agent. Conclusion: Significant cerebrovascular activity of S-Amlodipine nicotinate (0.1 mg/kg i/v) antihypertensive agent was revealed. The presence of GABAergic mechanism on cerebral blood flow in the agent action along with blockade of slow calcium channels ensures its high efficacy in treatment of both ischemic and hemorrhagic brain injuries.

Prolonged retention of the anorectic cobalt protoporphyrin in the hypothalamus and the resulting expression of Fos

2004 ◽  
Vol 287 (2) ◽  
pp. R465-R471 ◽  
Author(s):  
Richard A. Galbraith ◽  
Ilean Hodgdon ◽  
Michele S. Grimm ◽  
Margaret A. Vizzard
Keyword(s):  
Male Rats ◽  
Halothane Anesthesia ◽  
Short Term ◽  
Brain Areas ◽  
Duration Of Action ◽  
Prolonged Duration ◽  
Cobalt Protoporphyrin ◽  
Prolonged Retention ◽  
The Brain

The anorectic cobalt protoporphyrin (CoPP) is known to elicit short-term hypophagia and long-term weight loss through unknown mechanisms in the brains of experimental animals. The goal of this work was to determine 1) if the prolonged duration of action of CoPP is related to its prolonged retention within the brain; and 2) with the use of immunohistochemical detection of Fos, the product of the early-immediate gene c-fos, which cells are activated after exposure to CoPP. These studies were carried out in male rats after intracerebroventricular administration of CoPP, 0.4 μmol/kg body wt, given under light halothane anesthesia. Residence of CoPP in the brain was determined by residual counts in dissected brains of 57CoPP-injected rats. Fos immunoreactivity was mapped in coronal sections of rat brains 4–6 h after injection with CoPP. The results showed that 57CoPP was retained in the hypothalamus preferentially compared with the cortex of the brain and could be detected in the hypothalamus for in excess of 5 wk. Fos activation was increased by CoPP, detected predominantly in neuronal rather than glial cells, and was markedly more robust in the hypothalamus than in other brain areas. Thus CoPP remains in the hypothalamus for prolonged periods and activates Fos expression in the hypothalamus.

scholarly journals Accessing neuroinflammation sites: Monocyte/neutrophil-mediated drug delivery for cerebral ischemia

2019 ◽  
Vol 5 (7) ◽  
pp. eaau8301 ◽  
Author(s):  
Jia Hou ◽  
Xu Yang ◽  
Shiyi Li ◽  
Zhekang Cheng ◽  
Yuhua Wang ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Blood Flow ◽  
Cerebral Ischemia ◽  
Inflammatory Response ◽  
Target Cells ◽  
Ischemic Brain ◽  
Therapeutic Molecules ◽  
Cerebral Parenchyma ◽  
Cell Carriers ◽  
The Brain

Cerebral ischemia (CI) results from inadequate blood flow to the brain. The difficulty of delivering therapeutic molecules to lesions resulting from CI hinders the effective treatment of this disease. The inflammatory response following CI offers a unique opportunity for drug delivery to the ischemic brain and targeted cells because of the recruitment of leukocytes to the stroke core and penumbra. In the present study, neutrophils and monocytes were explored as cell carriers after selectively carrying cRGD liposomes, which effectively transmigrated the blood-brain barrier, infiltrated the cerebral parenchyma, and delivered therapeutic molecules to the injured sites and target cells. Our results showed the successful comigration of liposomes with neutrophils/monocytes and that both monocytes and neutrophils were important for successful delivery. Enhanced protection against ischemic injury was achieved in the CI/reperfusion model. The strategy presented here shows potential in the treatment of CI and other diseases related to inflammation.

scholarly journals RheoSens; RheoPatch

2020 ◽  
Author(s):  
Tariq H. Khan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Minimally Invasive ◽  
Brain Injuries ◽  
Tissue Oxygenation ◽  
Traumatic Brain Injuries ◽  
Invasive Device ◽  
The Brain ◽  
Minimally Invasive Device

Rheo Probe is a minimally invasive device, implanted in the brain matter for patients in a coma following brain haemorrage or traumatic brain injuries to measure cerebral blood flow, intracranial pressure, temperature and oxygenation parameters. Nearinfrared sensors assess levels of tissue oxygenation as well as cerebral blood flow by measuring oxygenated and deoxygenated hemoglobin based on spectrometry.

scholarly journals Violation in the axis of the "microbiota of the digestive tract-brain" under conditions of ischemia-reperfusion of the brain (literature review)

2021 ◽  
Vol 11 (5) ◽  
pp. 325-332
Author(s):  
O. Tkachuk ◽  
S. Tkachuk ◽  
M. Povar ◽  
O. Denysenko ◽  
V. Shtefaniuk
Keyword(s):  
Literature Review ◽  
Intestinal Microbiota ◽  
Brain Injuries ◽  
Ischemia Reperfusion ◽  
T Cell Homeostasis ◽  
Ischemic Brain ◽  
Intestinal Lymphocytes ◽  
And Migration ◽  
The Brain

The aim of the study is to analyze current views concerning interrelations between the state of intestinal microbiota and the course of ischemic-reperfusion brain injury.   Conclusion. Literary data are indicative of disputable scientific opinions existing nowadays concerning the role of dysbacteriosis (neuroprotective or neurodegenerative) in the course of ischemic brain injuries. Meanwhile, the studies are in common concerning the evidenced role of the intestinal microbiota in disturbances of T-cell homeostasis, ratio changes of their Treg-Th17 subpopulations, and migration of intestinal lymphocytes to the ischemic brain.  

scholarly journals Functional features of hemodynamic changes in preterm kids in residual period of development

2018 ◽  
pp. 71-74
Author(s):  
L. E. Vigovskaya ◽  
A. R. Gaynutdinov
Keyword(s):  
Blood Flow ◽  
Preterm Infants ◽  
Premature Infants ◽  
Cerebrovascular Disorders ◽  
Birth Trauma ◽  
Trigger Factor ◽  
Hemodynamic Changes ◽  
Flow Through ◽  
Functional Features ◽  
The Brain

Results of dopplerographic studies have delineate the severity of cerebrovascular disorders in different categories of preterm infants. The most significant hemodynamic changes characteristic for extremely premature infants, regardless of severity of the condition at birth, which is manifested as a decrease in blood flow through the main vessels of the head and neck, especially pronounced disturbances in the venous system of the brain. Birth trauma is a trigger factor in the implementation of hemodynamic disorders of the brain in these patients.

scholarly journals Circulating Tight-Junction Proteins Are Potential Biomarkers for Blood-Brain Barrier Function in a Model of Neonatal Hypoxic/Ischemic Brain Injury

2020 ◽  
Author(s):  
Axel Erik Andersson ◽  
Carina Mallard ◽  
Carl Joakim Ek
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Injuries ◽  
Brain Barrier ◽  
Neonatal Brain ◽  
Ischemic Brain ◽  
Blood Brain ◽  
Hypoxia Ischemia ◽  
The Brain ◽  
Junction Proteins

Abstract BackgroundNeonatal hypoxia-ischemia often leads to lifelong disabilities with limited treatments currently available. The brain vasculature is an important factor in many neonatal brain pathologies but there is a lack of diagnostic tools to evaluate the brain vascular health of neonates in a clinical setting. Measurement of blood-brain barrier tight-junction proteins have shown promise as biomarkers for brain injury in the adult. Here we tested the biomarker potential of tight-junctions in the context of neonatal brain injury.MethodsThe levels of TJ-proteins (occluding, claudin-5, and zonula occludens-1) in both blood plasma and cerebrospinal fluid (CSF) as well as blood-brain barrier function were measured in a clinically relevant hypoxia/ischemia model in neonatal rats.ResultsTemporally acute elevated levels of occludin and claudin-5 could be measured in blood and CSF after hypoxia/ischemia with males generally having higher levels than females. The levels of claudin-5 in CSF correlated with the severity of the brain injury at 24h post- hypoxia/ischemia. Simultaneously, we detected early increase in blood-brain barrier-permeability at 6 and 24h after hypoxia/ischemia.ConclusionsLevels of circulating claudin-5 and occludin are increased after hypoxic/ischemic brain injuries and blood-brain barrier-impairment and have promise as early biomarkers for cerebral vascular health and as a tool for risk assessment of neonatal brain injuries.

scholarly journals Circulating tight-junction proteins are potential biomarkers for blood–brain barrier function in a model of neonatal hypoxic/ischemic brain injury

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
E. Axel Andersson ◽  
Carina Mallard ◽  
C. Joakim Ek
Keyword(s):  
Brain Injury ◽  
Blood Brain Barrier ◽  
Brain Injuries ◽  
Vascular Dysfunction ◽  
Brain Barrier ◽  
Neonatal Brain ◽  
Ischemic Brain ◽  
Blood Brain ◽  
Hypoxia Ischemia ◽  
The Brain

Abstract Background Neonatal encephalopathy often leads to lifelong disabilities with limited treatments currently available. The brain vasculature is an important factor in many neonatal neurological disorders but there is a lack of diagnostic tools to evaluate the brain vascular dysfunction of neonates in the clinical setting. Measurement of blood–brain barrier tight-junction (TJ) proteins have shown promise as biomarkers for brain injury in the adult. Here we tested the biomarker potential of tight-junctions in the context of neonatal brain injury. Methods The levels of TJ-proteins (occluding, claudin-5, and zonula occludens protein 1) in both blood plasma and cerebrospinal fluid (CSF) as well as blood–brain barrier function via 14C-sucrose (342 Da) and Evans blue extravasation were measured in a hypoxia/ischemia brain-injury model in neonatal rats. Results Time-dependent changes of occludin and claudin-5 levels could be measured in blood and CSF after hypoxia/ischemia with males generally having higher levels than females. The levels of claudin-5 in CSF correlated with the severity of the brain injury at 24 h post- hypoxia/ischemia. Simultaneously, we detected early increase in blood–brain barrier-permeability at 6 and 24 h after hypoxia/ischemia. Conclusions Levels of circulating claudin-5 and occludin are increased after hypoxic/ischemic brain injuries and blood–brain barrier-impairment and have promise as early biomarkers for cerebral vascular dysfunction and as a tool for risk assessment of neonatal brain injuries.

Neuroprotective Effects of Long-Term Metformin Preconditioning on Rats with Ischemic Brain Injuries

2021 ◽  
pp. 1-7
Author(s):  
Lu Wang ◽  
Aqian Wang ◽  
Hongtao Guo ◽  
Zhenxian Zhang ◽  
Shenghai Wang ◽  
...  
Keyword(s):  
Sham Group ◽  
Brain Injuries ◽  
Beclin 1 ◽  
Pathological Changes ◽  
Neuroprotective Effects ◽  
Ischemic Brain ◽  
Infarct Area ◽  
The Brain ◽  
Apoptosis Level

<b><i>Introduction:</i></b> This study is to analyze the neuroprotective effects of long-term metformin (Met) preconditioning on rats with ischemic brain injuries and the related mechanisms. <b><i>Methods:</i></b> Twenty-five Sprague-Dawley rats were randomly divided into 5 groups: sham group, middle cerebral artery occlusion (MCAO) group, normal saline + MCAO group, pre- Met + MCAO group, and 3-MA + Met + MCAO group. Pathological changes of brain were observed by hematoxylin-eosin staining. Neurobehavior scores were calculated. Infarct area was assessed by 2,3,5-triphenyltetrazolium chloride staining. Apoptosis of neurons was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL). Western blot tested the expression of LC3 (microtubule-associated protein 1 light chain 3), Beclin-1, adenosine 5′-monophosphate ([AMP]-activated protein kinase [AMPK]), and p-AMPK in hippocampal CA1 region. <b><i>Results:</i></b> Compared with the sham group, the MCAO group induced severe pathological changes in the brain. The neurobehavior scores and infarct area in the brain were increased in the MCAO group than in the sham group. The apoptosis level in the MCAO group was also higher than in the sham group. However, after pretreatment with Met, the pathological changes in the brain were attenuated. Compared with the MCAO group, the pre-Met + MCAO group also had decreased neurobehavior scores and infarct area in the brain. Additionally, the apoptosis level in the pre-Met + MCAO group was lower than in the MCAO group. Moreover, the MCAO group had increased levels of LC3 and Beclin-1 than in the sham group. In the pre-Met + MCAO group, their levels were decreased than in the MCAO group. The p-AMPK level in the pre-Met + MCAO group was also increased than in the MCAO group, suggesting activation of p-AMPK by Met. <b><i>Conclusion:</i></b> Long-term Met pretreatment has neuroprotective effect on ischemic brain injury, which may be related to the regulation of autophagy-related protein expression and apoptosis.

scholarly journals Lipopolysaccharide Worsens the Prognosis of Experimental Cerebral Ischemia via Interferon Gamma-Induced Protein 10 Recruit in the Acute Stage

2019 ◽  
Author(s):  
Ping Wang ◽  
Jiaqi ZHANG ◽  
Feifei GUO ◽  
Shuang Wang ◽  
Yi ZHANG ◽  
...  
Keyword(s):  
Brain Injury ◽  
Interferon Gamma ◽  
Infarct Volume ◽  
Brain Homogenate ◽  
Acute Stage ◽  
Male Rats ◽  
Ischemic Brain Injury ◽  
Ppi Network ◽  
Ischemic Brain ◽  
The Brain

Abstract Background: Infection is an important clinical complication facing stroke-patients and triples the risk of death within 30 days post-stroke via mechanisms which are poorly understood. Aims: We tried to explore the mechanisms that inflammation caused by infections aggravated the ischemic brain injury after middle cerebral artery occlusion (MCAO). Methods: We used lipopolysaccharide (LPS) as systemic inflammatory stimuli to explore the mechanisms of aggravated ischemic brain injury after Sprague-Dawley male rats subjected to MCAO.Brain damage was evaluated by cerebral blood perfusion, Longa-5 scores, infarct volume and edema degree. Systemic cytokine responses and inflammatory changes in the plasma and brain were analyzed by ELISA kit, RT 2 Profiler TM PCR array, and quantitative real-time PCR.The differential genes were subjected to Gene Ontology enrichment analysis and Protein-Protein interaction (PPI) network construction. Results: LPS profoundly aggravated the brain damage after 24 hrs post-MCAO. At the acute stage (Ischemia/Reperfusion 90min/3h), the brain homogenate gene expression of Interleukin 6 (IL-6), Tumor necrosis factor a(TNF-a), Interleukin 1b(IL-1b)and Interferon Gamma-Induced Protein 10 (IP-10)was significantly up-regulated and the contents in plasma and brain homogenate were significantly increased in MCAO and MCAO+LPS group. IP-10 was the only gene with significant difference between MCAO and MCAO+LPS group, which was also in an important position with degrees of ³14 in PPI network. Conclusions: It was possible that trace LPS aggravated the ischemic brain injury by induction of excessive IP-10 secretion in the acute stage, leading to excessive inflammatory response, which consequently increased the infarct volume and edema degree 24 hrs post-MCAO.

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