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Tytuł pozycji:

Exacerbation of blood-brain barrier breakdown, edema formation, nitric oxide synthase upregulation and brain pathology after heat stroke in diabetic and hypertensive rats. Potential neuroprotection with cerebrolysin treatment.

Tytuł :
Exacerbation of blood-brain barrier breakdown, edema formation, nitric oxide synthase upregulation and brain pathology after heat stroke in diabetic and hypertensive rats. Potential neuroprotection with cerebrolysin treatment.
Autorzy :
Muresanu DF; Department of Clinical Neurosciences, University of Medicine & Pharmacy, Cluj-Napoca, Romania; 'RoNeuro' Institute for Neurological Research and Diagnostic, Cluj-Napoca, Romania.
Sharma A; International Experimental Central Nervous System Injury & Repair (IECNSIR), Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden.
Patnaik R; International Experimental Central Nervous System Injury & Repair (IECNSIR), Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden; Department of Biomaterials, School of Biomedical Engineering, Institute of technology, Banaras Hindu University, Varanasi, India; Indian Institute of Technology, Banaras Hindu University, Varanasi, India.
Menon PK; International Experimental Central Nervous System Injury & Repair (IECNSIR), Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden; Indian Institute of Technology, Banaras Hindu University, Varanasi, India.
Mössler H; Ever NeuroPharma, Oberburgau, Austria.
Sharma HS; International Experimental Central Nervous System Injury & Repair (IECNSIR), Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, Uppsala University Hospital, Uppsala University, Uppsala, Sweden. Electronic address: .
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Źródło :
International review of neurobiology [Int Rev Neurobiol] 2019; Vol. 146, pp. 83-102. Date of Electronic Publication: 2019 Jul 18.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Original Publication: New York Ny : Academic Press
MeSH Terms :
Amino Acids/*pharmacology
Blood-Brain Barrier/*metabolism
Brain/*pathology
Brain Edema/*physiopathology
Diabetes Mellitus, Experimental/*prevention & control
Heat Stroke/*pathology
Heat Stroke/*physiopathology
Hypertension/*prevention & control
Nitric Oxide Synthase/*biosynthesis
Animals ; Brain/metabolism ; Diabetes Mellitus, Experimental/complications ; Hypertension/complications ; Male ; Neuroprotection/drug effects ; Rats ; Streptozocin ; Up-Regulation
Contributed Indexing :
Keywords: Blood-brain barrier*; Brain edema*; Brain pathology*; Cerebrolysin*; Diabetes*; Heat stress*; Hypertension*; Nitric oxide*
Substance Nomenclature :
0 (Amino Acids)
37KZM6S21G (cerebrolysin)
5W494URQ81 (Streptozocin)
EC 1.14.13.39 (Nitric Oxide Synthase)
Entry Date(s) :
Date Created: 20190728 Date Completed: 20200203 Latest Revision: 20200203
Update Code :
20210210
DOI :
10.1016/bs.irn.2019.06.007
PMID :
31349933
Czasopismo naukowe
There is a growing trend of hypertension among military and civilian populations due to lifetime stressful situations. If hypertension is uncontrolled it leads to development of diabetes and serious neurological complications. Most of the World populations live in temperate zone across the World. Thus, a possibility exists that these hypertensive and diabetic people may have external heat as potential risk factors for brain damage. We have seen brain edema and brain damage following exposure to heat stress at 38°C for 4h. A possibility exists that heat exposure in diabetic-hypertensive (DBHY) cases exacerbates exacerbation of brain pathology and edema formation. This hypothesis is examined in a rat model. The role of nitric oxide (NO) in exacerbation of HS-induced brain pathology was also evaluated using nitric oxide synthase (NOS) immunoreactivity. Hypertensive rats (produced by two-kidney one clip (2K1C) method) were made diabetic with streptozotocine (50mg/kg, i.p./day for 3days) treatment. After 6weeks, DBHY rats show 20-30mM/L Blood Glucose and hypertension (180-200mmHg). Subjection of these rats to 4h HS resulted in six- to eightfold higher BBB breakdown, brain edema formation and brain pathology. At this time, neuronal or inducible NOS expression was four- to sixfold higher in DBHY rats compared to controls. Interestingly, iNOS expression was higher than nNOS in DBHY rats. Cerebrolysin in high doses (10-mL/kg, i.v. instead of 5-mL/kg) induced significant neuroprotection and downregulation of nNOS and iNOS in DBHY animals whereas normal animals need only 5-mL/kg doses for this purpose. Our observations demonstrate that co-morbidly factors exacerbate brain damage in HS through NOS expression and require double dose of cerebrolysin for neuroprotection as compared to normal rats, not reported earlier.
(© 2019 Elsevier Inc. All rights reserved.)

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