Partial replacement of K+ with RB+ in the rat brain in vivo does not change the tissue potassium dynamics after focal cerebral ischemia and is detectable by 87Rb MRI

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S279-S279
Author(s):  
Victor E Yushmanov ◽  
Alexander Kharlamov ◽  
Eli J Wasserman ◽  
Fernando E Boada ◽  
Stephen C Jones
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Focal Cerebral Ischemia ◽  
Partial Replacement ◽  
Potassium Dynamics

In vivo optical reflectance imaging of spreading depression waves in rat brain with and without focal cerebral ischemia

2006 ◽  
Vol 11 (3) ◽  
pp. 034002 ◽  
Author(s):  
Shangbin Chen ◽  
Zhe Feng ◽  
Pengcheng Li ◽  
Steven L. Jacques ◽  
Shaoqun Zeng ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Spreading Depression ◽  
Focal Cerebral Ischemia ◽  
Optical Reflectance

scholarly journals Neuroprotection by Brazilian Green Propolis againstIn vitroandIn vivoIschemic Neuronal Damage

2005 ◽  
Vol 2 (2) ◽  
pp. 201-207 ◽  
Author(s):  
Masamitsu Shimazawa ◽  
Satomi Chikamatsu ◽  
Nobutaka Morimoto ◽  
Satoshi Mishima ◽  
Hiroichi Nagai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Neuronal Damage ◽  
Focal Cerebral Ischemia ◽  
Brain Infarction ◽  
Folk Medicine ◽  
Neuroprotective Function ◽  
Brazilian Green Propolis

We examined whether Brazilian green propolis, a widely used folk medicine, has a neuroprotective functionin vitroand/orin vivo.In vitro, propolis significantly inhibited neurotoxicity induced in neuronally differentiated PC12 cell cultures by either 24 h hydrogen peroxide (H2O2) exposure or 48 h serum deprivation. Regarding the possible underlying mechanism, propolis protected against oxidative stress (lipid peroxidation) in mouse forebrain homogenates and scavenged free radicals [induced by diphenyl-p-picrylhydrazyl (DPPH). In micein vivo, propolis [30 or 100 mg/kg; intraperitoneally administered four times (at 2 days, 1 day and 60 min before, and at 4 h after induction of focal cerebral ischemia by permanent middle cerebral artery occlusion)] reduced brain infarction at 24 h after the occlusion. Thus, a propolis-induced inhibition of oxidative stress may be partly responsible for its neuroprotective function againstin vitrocell death andin vivofocal cerebral ischemia.

Selenoprotein S expression in the rat brain following focal cerebral ischemia

2013 ◽  
Vol 34 (9) ◽  
pp. 1671-1678 ◽  
Author(s):  
Li Xia Liu ◽  
Xue Ying Zhou ◽  
Cheng Shan Li ◽  
Li Qing Liu ◽  
Shan Ying Huang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Rat Brain ◽  
Focal Cerebral Ischemia ◽  
Selenoprotein S

scholarly journals Leukocyte-Endothelium Interactions during Permanent Focal Cerebral Ischemia in Mice

2004 ◽  
Vol 24 (6) ◽  
pp. 668-676 ◽  
Author(s):  
Hiroharu Kataoka ◽  
Seong-Woong Kim ◽  
Nikolaus Plesnila
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Molecular Mechanisms ◽  
Focal Cerebral Ischemia ◽  
Fluorescent Microscopy ◽  
Capillary Density ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
Adherent Leukocytes

The contribution of leukocyte infiltration to brain damage after permanent focal cerebral ischemia and the underlying molecular mechanisms are still unclear. Therefore, the aim of this study was to establish a mouse model for the visualization of leukocytes in the cerebral microcirculation in vivo and to investigate leukocyte-endothelial interaction (LEI) after permanent middle cerebral artery occlusion (MCAO). Sham-operated 129/Sv mice showed physiologic LEI in pial venules as observed by intravital fluorescent microscopy. Permanent focal cerebral ischemia induced a significant increase of LEI predominantly in pial venules. The number of rolling and adherent leukocytes reached 36.5 ± 13.2/100 μm × min and 22.5 ± 7.9/100 μm × min, respectively at 120 minutes after MCAO ( P = 0.016 vs. control). Of note, rolling and adherent leukocytes were also observed in arterioles of ischemic animals (7.3 ± 3.0/100 μm × min rolling and 3.0 ± 3.6/100 μm × min adherent). Capillary density was not different between groups. These results demonstrate that leukocytes accumulate in the brain not only after transient but also after permanent focal cerebral ischemia and may therefore contribute to brain damage after stroke without reperfusion.

scholarly journals In Vivo Microdialysis of Endogenous and 13C-labeled TCA Metabolites in Rat Brain: Reversible and Persistent Effects of Mitochondrial Inhibition and Transient Cerebral Ischemia

Metabolites ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 204 ◽  
Author(s):  
Jesper F. Havelund ◽  
Kevin H. Nygaard ◽  
Troels H. Nielsen ◽  
Carl-Henrik Nordström ◽  
Frantz R. Poulsen ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mitochondrial Dysfunction ◽  
Rat Brain ◽  
De Novo ◽  
Tricarboxylic Acid Cycle ◽  
Experimental Models ◽  
Transient Cerebral Ischemia ◽  
Metabolic Disturbances ◽  
Metabolic Marker

Cerebral micro-dialysis allows continuous sampling of extracellular metabolites, including glucose, lactate and pyruvate. Transient ischemic events cause a rapid drop in glucose and a rise in lactate levels. Following such events, the lactate/pyruvate (L/P) ratio may remain elevated for a prolonged period of time. In neurointensive care clinics, this ratio is considered a metabolic marker of ischemia and/or mitochondrial dysfunction. Here we propose a novel, sensitive microdialysis liquid chromatography-mass spectrometry (LC-MS) approach to monitor mitochondrial dysfunction in living brain using perfusion with 13C-labeled succinate and analysis of 13C-labeled tricarboxylic acid cycle (TCA) intermediates. This approach was evaluated in rat brain using malonate-perfusion (10–50 mM) and endothelin-1 (ET-1)-induced transient cerebral ischemia. In the malonate model, the expected changes upon inhibition of succinate dehydrogenase (SDH) were observed, i.e., an increase in endogenous succinate and decreases in fumaric acid and malic acid. The inhibition was further elaborated by incorporation of 13C into specific TCA intermediates from 13C-labeled succinate. In the ET-1 model, increases in non-labeled TCA metabolites (reflecting release of intracellular compounds) and decreases in 13C-labeled TCA metabolites (reflecting inhibition of de novo synthesis) were observed. The analysis of 13C incorporation provides further layers of information to identify metabolic disturbances in experimental models and neuro-intensive care patients.

scholarly journals A Strategic Application of Fast Fourier Transform as a Novel Tool to Evaluate the Extent of Neuronal Insult in Rat Model of Focal Cerebral Ischemia

2013 ◽  
Vol 5 (1) ◽  
pp. 29-36 ◽  
Author(s):  
S Paul ◽  
P Bhattacharya ◽  
AK Pandey ◽  
N Sharma ◽  
JP Tiwari ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Animal Model ◽  
Spectral Analysis ◽  
Cerebral Ischemia ◽  
Rat Brain ◽  
Brain Function ◽  
Focal Cerebral Ischemia ◽  
Physiological State ◽  
Analysis Methods ◽  
Eeg Data

The present work envisages mathematical modeling of induced focal cerebral ischemia in animal model using EEG data with the help of Fast Fourier Transformation method. Amongst several analysis methods, spectral analysis methods are important because it detects the frequencies and characteristics changes of brain waveforms depending on the brain function affected from disorders and physiological state. There are many applications of FFT, and the most important being that it is one of the basic conventional spectral analysis methods. However, it has some limitations, for instance, it adds contributions in the low frequency region which are not present in the original signal, and necessitates the use of windowing for decreasing the error rate. The present analysis was undertaken to ensure actual correlation of the different mathematical paradigms. EEG data were obtained from different regions of rat brain and were processed by FFT modeling in MATLAB platform. The assessment of long lasting functional outcome and to prevalent classical approach to study stroke was necessitated and therefore highly recommended to evaluate the efficacy of therapeutic strategies in relation to EEG in animal model of brain stroke. This mathematical modeling specifically Power Spectrum Density analysis was done to correlate the different prevalent condition of rat brain function. DOI: http://dx.doi.org/10.3329/bjmp.v5i1.14666 Bangladesh Journal of Medical Physics Vol.5 No.1 2012 29-36

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