Neuroprotective Effect of Mild Hypothermia in Experimental Brain Ischemia

2000 ◽  
pp. 69-82
Author(s):  
Hisato Yanase ◽  
Kiyoshi Kataoka
Keyword(s):  
Brain Ischemia ◽  
Mild Hypothermia ◽  
Neuroprotective Effect

scholarly journals Neuroprotective effect of mild hypothermia in the temporary brain ischemia in cats

2007 ◽  
Vol 65 (3b) ◽  
pp. 810-815 ◽  
Author(s):  
Hiroshi Nakano ◽  
Benedicto Oscar Colli ◽  
Luiza da Silva Lopes
Keyword(s):  
Basal Ganglia ◽  
Brain Ischemia ◽  
Mild Hypothermia ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Focal Ischemia ◽  
Volume Calculation ◽  
Significant Difference ◽  
Group 2 ◽  
Group 1

OBJECTIVE: To evaluate the neuroprotective effect of mild hypothermia during temporary focal ischemia in cats. METHOD: 20 cats underwent middle cerebral artery 60 minutes occlusion and 24 hours reperfusion: 10 under normothermia and 10 under mild hypothermia (32º C). Brain coronal sections 2mm thick were stained with 2,3,5-triphenyltetrazolium hydrochloride, photographed and evaluated with software for volume calculation. RESULTS:Cortical ischemia was found in 7 and basal ganglia ischemia in 8 animals of group 1 and in both regions in 5 animals of group 2 (no difference: p=0.6499 for cortical; p=0.3498 for basal ganglia). No ischemia was found in 5 animals of group 2 and in none of group 1 (significant difference, p=0.0325). The infarct volume was greater in group 1 than 2 (p=0.0433). CONCLUSION: Mild hypothermia did not interfere with location of ischemia, but it was effective for reducing the infarct volume.

scholarly journals The hypoxia sensitive metal transcription factor MTF-1 activates NCX1 brain promoter and participates in remote postconditioning neuroprotection in stroke

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Valeria Valsecchi ◽  
Giusy Laudati ◽  
Ornella Cuomo ◽  
Rossana Sirabella ◽  
Lucio Annunziato ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Brain Ischemia ◽  
Femoral Artery ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Artery Occlusion ◽  
Sodium Calcium Exchanger ◽  
Protein Levels ◽  
Relevant Role ◽  
Remote Postconditioning

AbstractRemote limb ischemic postconditioning (RLIP) is an experimental strategy in which short femoral artery ischemia reduces brain damage induced by a previous harmful ischemic insult. Ionic homeostasis maintenance in the CNS seems to play a relevant role in mediating RLIP neuroprotection and among the effectors, the sodium-calcium exchanger 1 (NCX1) may give an important contribution, being expressed in all CNS cells involved in brain ischemic pathophysiology. The aim of this work was to investigate whether the metal responsive transcription factor 1 (MTF-1), an important hypoxia sensitive transcription factor, may (i) interact and regulate NCX1, and (ii) play a role in the neuroprotective effect mediated by RLIP through NCX1 activation. Here we demonstrated that in brain ischemia induced by transient middle cerebral occlusion (tMCAO), MTF-1 is triggered by a subsequent temporary femoral artery occlusion (FAO) and represents a mediator of endogenous neuroprotection. More importantly, we showed that MTF-1 translocates to the nucleus where it binds the metal responsive element (MRE) located at −23/−17 bp of Ncx1 brain promoter thus activating its transcription and inducing an upregulation of NCX1 that has been demonstrated to be neuroprotective. Furthermore, RLIP restored MTF-1 and NCX1 protein levels in the ischemic rat brain cortex and the silencing of MTF-1 prevented the increase of NCX1 observed in RLIP protected rats, thus demonstrating a direct regulation of NCX1 by MTF-1 in the ischemic cortex of rat exposed to tMCAO followed by FAO. Moreover, silencing of MTF-1 significantly reduced the neuroprotective effect elicited by RLIP as demonstrated by the enlargement of brain infarct volume observed in rats subjected to RLIP and treated with MTF-1 silencing. Overall, MTF-dependent activation of NCX1 and their upregulation elicited by RLIP, besides unraveling a new molecular pathway of neuroprotection during brain ischemia, might represent an additional mechanism to intervene in stroke pathophysiology.

scholarly journals Our experiences with therapeutic hypothermia

2007 ◽  
Vol 60 (9-10) ◽  
pp. 431-435 ◽  
Author(s):  
Milovan Petrovic ◽  
Ilija Srdanovic ◽  
Gordana Panic ◽  
Tibor Canji ◽  
Tihomir Miljevic
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Neurological Outcome ◽  
Mild Hypothermia ◽  
Acute Myocarditis ◽  
Neuroprotective Effect ◽  
Sudden Cardiac Arrest ◽  
Neurological Recovery ◽  
Global Cerebral Ischemia ◽  
Resuscitation Guidelines

Introduction. The single most important clinically relevant cause of global cerebral ischemia is cardiac arrest. The estimated rate of sudden cardiac arrest is between 40 and 130 cases per 100.000 people per year. Almost 80% of patients initially resuscitated from cardiac arrest remain comatose for more than one hour. One year after cardiac arrest only 10-30% of these patients survive with good neurological outcome. The ability to survive anoxic no-flow states is dramatically increased with protective and preservative hypothermia. The results of clinical studies show a marked neuroprotective effect of mild hypothermia in resuscitation. Material and Methods. In our clinic, 12 patients were treated with therapeutic hypothermia. A combination of intravascular and external method of cooling was used according to the ILCOR (International Liaison Committee on Resuscitation) guidelines. The target temperature was 33oC, while the duration of cooling was 24 hours. After that, passive rewarming was allowed. All patients also received other necessary therapy. Results. Six patients (50%) had a complete neurological recovery. Two patients (16.6%) had partial neurological recovery. Four patients (33.3%) remained comatose. Five patients (41.66%) survived, while 7 (58.33%) patients died. The main cause of cardiac arrest was acute myocardial infarction (91.6%). One patient had acute myocarditis. Conclusion. Mild resuscitative hypothermia after cardiac arrest improves neurological outcome and reduces mortality in comatose survivors. .

scholarly journals Dose Effect Evaluation and Therapeutic Window of the Neuro-EPO Nasal Application for the Treatment of the Focal Ischemia Model in the Mongolian Gerbil

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Iliana Sosa Teste ◽  
Yuneidys Mengana Tamos ◽  
Yamila Rodríguez Cruz ◽  
Adriana Muñoz Cernada ◽  
Janette Cruz Rodríguez ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Mongolian Gerbil ◽  
Neuroprotective Effect ◽  
Developed Countries ◽  
Focal Ischemia ◽  
Exploratory Activity ◽  
Dose Effect ◽  
Therapeutic Window ◽  
Average Dose ◽  
Thalamic Nuclei

Cerebrovascular disease is the third leading cause of death and the leading cause of disability in Cuba and in several developed countries. A possible neuroprotective agent is the rHu-EPO, whose effects have been demonstrated in models of brain ischemia. The Neuro-EPO is a derivative of the rHu-EPO that avoids the stimulation of erythropoiesis. The aim of this study was to determine the Neuro-EPO delivery into the central nervous system (CNS) to exert a neuroprotective effect in cerebral ischemia model of the Mongolian gerbil. The Neuro-EPO in a rate of 249.4 UI every 8 hours for 4 days showed 25% higher viability efficacy (), improving neurological score and behavior of the spontaneous exploratory activity, the preservation of CA3 areas of the hippocampus, the cortex, and thalamic nuclei in the focal ischemia model of the Mongolian gerbil. In summary, this study, the average dose-used Neuro-EPO (249.4 UI/10 μL/every 8 hours for 4 days), proved to be valid indicators of viability, neurological status, and spontaneous exploratory activity, being significantly lower than that reported for the systemically use of the rHu-EPO as a neuroprotectant. Indeed, up to 12 h after brain ischemia is very positive Neuro-EPO administration by the nasal route as a candidate for neuroprotection.

Glucosamine exerts a neuroprotective effect via suppression of inflammation in rat brain ischemia/reperfusion injury

Glia ◽  
2010 ◽  
Vol 58 (15) ◽  
pp. 1881-1892 ◽  
Author(s):  
So-Young Hwang ◽  
Joo-Hyun Shin ◽  
Ji-Sun Hwang ◽  
Song-Yi Kim ◽  
Jin-A Shin ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Rat Brain ◽  
Brain Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion

Neuroprotective effect of oral choline administration after global brain ischemia in rats

2014 ◽  
Vol 18 (6) ◽  
pp. 265-274 ◽  
Author(s):  
Andrea Aurélio Borges ◽  
Philipe Nicolas EI-Batah ◽  
Lilia Fumie Yamashita ◽  
Aline dos Santos Santana ◽  
Antonio Carlos Lopes ◽  
...  
Keyword(s):  
Brain Ischemia ◽  
Neuroprotective Effect ◽  
Global Brain Ischemia ◽  
Global Brain

scholarly journals N-Stearoyl-L-Tyrosine Inhibits the Senescence of Neural Stem/Progenitor Cells Induced by Aβ1–42via the CB2 Receptor

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Wen-Qing Li ◽  
Ze-jian Wang ◽  
Sha Liu ◽  
Yue Hu ◽  
Ming Yin ◽  
...  
Keyword(s):  
Stem Cells ◽  
Progenitor Cells ◽  
Brain Ischemia ◽  
Neuroprotective Effect ◽  
Cb1 Receptors ◽  
Cb2 Receptor ◽  
Positive Rate ◽  
Neural Stem Progenitor Cells ◽  
Chronic Brain Ischemia

Alzheimer’s disease, one of the neurodegenerative diseases, shows the progressive senescence of neural progenitor/stem cells. N-Stearoyl-L-tyrosine (NsTyr) showed neuroprotective effect against chronic brain ischemia in previous reports. In the present study, we find the antisenescent effects of NsTyr-2K in NSPCs induced by Aβ1–42in vitro. Cell viability of NSPCs was evaluated by CCK8 assay; SA-β-gal staining was used to evaluate senescence of NSPCs. CB receptors were detected by immunohistochemistry in NSPCs. AM251 or AM630 was used to offset the anti-senescence effects afforded by NsTyr-2K. The positive rate of SA-β-gal staining was significantly increased in NSPCs after incubation with Aβ1–42for 9 days. CB receptors were found on the surface of NSPCs. The expression level of CB1 receptors was significantly decreased in NSPCs after incubation with Aβ1–42. This phenomenon was reversed dose-dependently by NsTyr-2K. NsTyr-2K attenuated Aβ1–42induced NSPCs senescence dose-dependently, and its antisenescence effect was completely abolished by AM630. Aβ1–42dose-dependently increased the prosenescence molecules p16 and Rb. Their expression was inhibited by NsTyr-2K dose-dependently and blocked by AM630 in NSPCs. These results suggest that NsTyr-2K can alleviate the senescence of NSPCs induced by Aβ1–42via CB2 receptor.

Involvement of mitochondria on neuroprotective effect of sphingosine-1-phosphate in cell death in an in vitro model of brain ischemia

2010 ◽  
Vol 470 (2) ◽  
pp. 130-133 ◽  
Author(s):  
Alba Agudo-López ◽  
Begoña G. Miguel ◽  
Inmaculada Fernández ◽  
Ana M. Martínez
Keyword(s):  
Cell Death ◽  
Brain Ischemia ◽  
In Vitro Model ◽  
Neuroprotective Effect ◽  
Sphingosine 1 Phosphate ◽  
Vitro Model
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