Cooling Penetration Surrounding an Intra-Parenchymal Cooling Probe in Hypothermia Treatment for Ischemia or Head Injury Patients: Theoretical Analyses

2004 ◽  
Author(s):  
Liang Zhu ◽  
Axel J. Rosengart
Keyword(s):  
Animal Model ◽  
Temperature Distribution ◽  
Cerebral Ischemia ◽  
Head Injury ◽  
Brain Tissue ◽  
Brain Ischemia ◽  
Clinical Studies ◽  
Neurological Outcome ◽  
Clinical Importance ◽  
Theoretical Analyses

Inducing hypothermia to brain tissue after brain ischemia or head injury has been demonstrated beneficial to the patients. Clinical studies have shown that even 1 or 2°C temperature reduction in brain tissue can be protective [Dietrich 1992]. On the contrary, fever-induced hyperthermia can worsen the neurological outcome in an animal model after cerebral ischemia. It is of clinical importance to understand the temperature distribution in brain during brain hypothermia.

scholarly journals Neuroprotective and cerebrovascular effects of endogenous N-Arachidonoyl-GABA and its putative Cox-2 metabolite – GABA conjugate with Prostaglandin E2

2021 ◽  
Vol 7 (3) ◽  
pp. 49-61
Author(s):  
Narine R. Mirzoyan ◽  
Nelly G. Khostikyan ◽  
Vahe S. Meliksetyan ◽  
Arpine A. Hakobyan ◽  
Tamara S. Gan’shina ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Prostaglandin E2 ◽  
Brain Tissue ◽  
Brain Ischemia ◽  
Cerebral Circulation ◽  
Transient Ischemia ◽  
Cox 2 ◽  
The Brain ◽  
Rat Brain Tissue

Introduction: The aim of the study was to compare the neuroprotective and cerebrovascular effects of bioactive, endogenous lipid – N-arachidonoyl-GABA (AA-GABA) and GABA conjugate with prostaglandin E2 (PGE2-GABA) by evaluation of a morphological state of rat brain tissue and lipofuscin levels under the condition of permanent focal brain ischemia, as well as cerebral circulation under the condition of global transient ischemia. Materials and methods: The study has been implemented using the models of the left middle cerebral artery occlusion (MCAO) and global transient ischemia of the brain. A morphological examination of the brain tissue, a registration of local blood flow by laser flowmeter, and quantitative measurement of lipofuscin by fluorescence spectroscopy were used. Results and discussion: AA-GABA and the putative COX-2 metabolite PGE2-GABA showed significant neuroprotective and cerebrovascular effects in rat models of global and focal cerebral ischemia. In the MCAO model, AA-GABA and PGE2-GABA at a dose of 2 mg/kg/day administered i.p. for 6 or 12 days led to: 1) significant restoration of neurons and glial cells with intracellular regeneration of cytoplasmic and nuclear structures, 2) decrease in brain tissue edema; 3) attenuated thrombosis and stasis, and 4) absence of large necrotic foci in rat brain tissue. AA-GABA and PGE2-GABA at the same dose prevented excessive accumulation of lipofuscin in both brain hemispheres in rats with MCAO. All the studied compounds increase cerebral blood circulation in rats subjected to global transient ischemia. However, the cerebrovascular effect of PGE2-GABA was superior to the activity of AA-GABA and all other tested compounds. AA-GABA and PGE2-GABA, unlike PGE2 and nimodipine, increase the cerebral blood flow in rats with global transient brain ischemia and have no influence on the intact animals. Apparently, the GABAergic vascular system of the brain is involved in the mechanisms of the neuroprotective action of AA-GABA and PGE2-GABA. Conclusion: For the first time, we demonstrated the ability of AA-GABA and its putative metabolite COX-2 PGE2-GABA to improve cerebral circulation, attenuate structural damage and lipofuscin accumulation during cerebral ischemia. The natural origin of AA-GABA, which possesses neuroprotective and cerebrovascular activity, as well as anti-aggregatory activity, allows considering AA-GABA as one of the endogenous protective factors in ischemic brain lesions. Graphical abstract:

scholarly journals Chronic Brain Ischemia: From Risk Factors to Cerebrovascular Complications

2021 ◽  
Vol 7 (6) ◽  
Author(s):  
F. Yusupov ◽  
Sh. Nurmatov ◽  
N. Abdykalykova ◽  
A. Yuldashev ◽  
M. Abdykadyrov
Keyword(s):  
Risk Factors ◽  
Cerebral Ischemia ◽  
Arterial Hypertension ◽  
Brain Tissue ◽  
Brain Ischemia ◽  
Chronic Cerebral Ischemia ◽  
Cerebrovascular Complications ◽  
Cerebral Blood Supply ◽  
Chronic Brain Ischemia ◽  
The Brain

Chronic cerebral ischemia is a polyetiological, chronic progressive dysfunction of the brain caused by diffuse and / or small focal damage to the brain tissue in conditions of prolonged insufficiency of cerebral blood supply. The review reflects the current understanding of chronic cerebral ischemia. The main pathogenetic mechanisms of the onset of chronic cerebral ischemia in patients with arterial hypertension, atherosclerosis and smoking are outlined.

Neuroprotection and Angiogenesis: Dual Role of Erythropoietin in Brain Ischemia

Physiology ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 225-229 ◽  
Author(s):  
Hugo H. Marti ◽  
Myriam Bernaudin ◽  
Edwige Petit ◽  
Christian Bauer
Keyword(s):  
Cerebral Ischemia ◽  
Growth Factor ◽  
Protective Effect ◽  
Brain Tissue ◽  
Brain Ischemia ◽  
Vessel Growth ◽  
The Brain ◽  
Indirect Protection ◽  
Brain Vessel

Erythropoietin, originally defined as an erythroid growth factor, is upregulated in the brain under conditions of hypoxia. So far, two functions have been identified for this locally produced cytokine: a direct protective effect on neuronal cells during cerebral ischemia and an indirect protection of brain tissue that could be provided by promoting brain vessel growth.

The immunomodulatory sphingosine 1-phosphate analog FTY720 reduces lesion size and improves neurological outcome in a mouse model of cerebral ischemia

2009 ◽  
Vol 389 (2) ◽  
pp. 251-256 ◽  
Author(s):  
Bozena Czech ◽  
Waltraud Pfeilschifter ◽  
Niloufar Mazaheri-Omrani ◽  
Marc André Strobel ◽  
Timo Kahles ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mouse Model ◽  
Neurological Outcome ◽  
Lesion Size ◽  
Sphingosine 1 Phosphate

scholarly journals Expression of NMDA receptor and microRNA-219 in rats submitted to cerebral ischemia associated with alcoholism

2017 ◽  
Vol 75 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Cristiane Iozzi Silva ◽  
Paulo Cézar Novais ◽  
Andressa Romualdo Rodrigues ◽  
Camila A.M. Carvalho ◽  
Benedicto Oscar Colli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Wistar Rats ◽  
Molecular Mechanisms ◽  
Inverse Correlation ◽  
Control Group ◽  
The Brain ◽  
Lower Expression ◽  
Control Sham

ABSTRACT Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs. Objective: To evaluate the microRNA-219 and NMDA expression in brain tissue and blood of animals subjected to cerebral ischemia associated with alcoholism. Methods: Fifty Wistar rats were divided into groups: control, sham, ischemic, alcoholic, and ischemic plus alcoholic. The expression of microRNA-219 and NMDA were analyzed by real-time PCR. Results: When compared to the control group, the microRNA-219 in brain tissue was less expressed in the ischemic, alcoholic, and ischemic plus alcoholic groups. In the blood, this microRNA had lower expression in alcoholic and ischemic plus alcoholic groups. In the brain tissue the NMDA gene expression was greater in the ischemic, alcoholic, and ischemic plus alcoholic groups. Conclusion: A possible modulation of NMDA by microRNA-219 was observed with an inverse correlation between them.

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