scholarly journals Grafted Neural Progenitor Cells Persist in the Injured Site and Differentiate Neuronally in a Rodent Model of Cardiac Arrest-Induced Global Brain Ischemia

2020 ◽  
Vol 29 (9) ◽  
pp. 574-585
Author(s):  
Patricia Meyer ◽  
Denis Grandgirard ◽  
Marika Lehner ◽  
Matthias Haenggi ◽  
Stephen L. Leib
Keyword(s):  
Cardiac Arrest ◽  
Progenitor Cells ◽  
Brain Ischemia ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Rodent Model ◽  
Global Brain Ischemia ◽  
Global Brain

Creatine kinase isoenzymes in human cerebrospinal fluid and brain.

1984 ◽  
Vol 30 (11) ◽  
pp. 1804-1806 ◽  
Author(s):  
W L Chandler ◽  
K J Clayson ◽  
W T Longstreth ◽  
J S Fine
Keyword(s):  
Cerebrospinal Fluid ◽  
Creatine Kinase ◽  
Cardiac Arrest ◽  
Brain Ischemia ◽  
Blood Contamination ◽  
Global Brain Ischemia ◽  
Qualitative And Quantitative ◽  
Human Cerebrospinal Fluid ◽  
Brain Extracts ◽  
Global Brain

Abstract Extracts of normal brains obtained at autopsy and cerebrospinal fluid (CSF) from patients with global brain ischemia were analyzed for creatine kinase (CK; EC 2.7.3.2) isoenzymes. We used both qualitative and quantitative assays (electrophoresis and immunoinhibition). Brain extracts contained CK-BB isoenzyme and mitochondrial CK. In 54 CSF samples free of blood contamination and with total activities ranging from 7 to 2010 U/L (mean 202 U/L), virtually all of the CK activity was due to CK-BB, and none to CK-MM or CK-MB. We conclude that brain contains CK-BB and mitochondrial CK, but lacks CK-MM and CK-MB. After cardiac arrest, CK-BB is released into the CSF. Any CK-MM in the CSF is probably from blood contamination, in which case immunoinhibition with anti-CK-M antibodies accurately quantifies CK-BB.

scholarly journals Uncoupled Cerebral Blood Flow and Metabolism after Severe Global Ischemia in Rats

1992 ◽  
Vol 12 (5) ◽  
pp. 802-808 ◽  
Author(s):  
Narendra C. Singh ◽  
Patrick M. Kochanek ◽  
Joanne K. Schiding ◽  
John A. Melick ◽  
Edwin M. Nemoto
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Brain Ischemia ◽  
Global Ischemia ◽  
Global Brain Ischemia ◽  
Sagittal Sinus ◽  
Postischemic Period ◽  
Baseline Values ◽  
Global Brain

In a rat model of complete global brain ischemia (neck tourniquet) lasting either 3 min or 20 min, we monitored global CBF (sagittal sinus H2 clearance) and CMRO2 for 6 h to test the hypothesis that delayed postischemic hyperemia and uncoupling of CBF and CMRO2 occur depending on the severity of the insult. Early postischemic hyperemia occurred in both the 3-min and 20-min groups ( p < 0.05 vs. baseline values) and resolved by 15 min. Hypoperfusion occurred in the 3-min group between 15 and 60 min postischemia (≈23% reduction), and in the 20-min group from 15 to 120 min postischemia (≈50% reduction) ( p < 0.05), and then resolved. CMRO2 was not significantly different from baseline at any time after ischemia in the 3-min group. After 20 min of ischemia, however, CMRO2 was decreased (≈60%) throughout the postischemic period ( p < 0.05). At 5 min after ischemia, CBF/CMRO2 was increased in both groups but returned to baseline from 60 to 120 min postischemia. In the 3-min group, CBF/CMRO2 remained at baseline throughout the rest of the experiment. However, in the 20-min group, CBF/CMRO2 once again increased (≈100%), reaching a significant level at 180 min and remaining so for the rest of the 6-h period ( p < 0.05). These data demonstrate biphasic uncoupling of CBF and CMRO2 after severe (20 min) global ischemia in rats. This relatively early reemergence of CBF/CMRO2 uncoupling after 180 min of reperfusion is similar to that observed after prolonged cardiac arrest and resuscitation in humans.

Abstract TP43: Transient Global Brain Ischemia Induces Striatal Neuronal Death of T1-Hyperintensity without Hemorrhage: Susceptibility-Weighted Imaging Study on Cardiac Arrest Survivors

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Masayuki Fujioka ◽  
Tomoo Watanabe ◽  
Toshiaki Taoka ◽  
Kazuo Okuchi
Keyword(s):  
Cardiac Arrest ◽  
Brain Ischemia ◽  
Neuronal Death ◽  
Late Onset ◽  
Global Brain Ischemia ◽  
Dorsolateral Striatum ◽  
Selective Neuronal Death ◽  
T1 Hyperintensity ◽  
Hemoglobin Degradation ◽  
Global Brain

Background: Global brain ischemia-reperfusion leads to selective neuronal death in the hippocampal CA1 area, cerebellar cortex, dorsolateral striatum, and/or neocortical layers 3, 5, and 6 in animal models and in humans. We have reported a delayed neurodegeneration of late-onset neuroimaging change in such brain areas vulnerable to ischemia (Stroke.1994;25:2091-95., Stroke.1999;30:1038-42., Stroke.1999;30:1043-46., Cerebrovasc Dis.2000;10:2-7., Ann Neurol.2003;54:732-7.). The magnetic resonance imaging (MRI) studies on patients after cardiac arrest showed 1) bilateral neurodegeneration with hyperintensity on T1-weighted MRI in the striatum, thalamus, and/or substantia nigra (Stroke.1994;25:2091-5., Neuroradiology.1994;36:605-7.), and 2) specific hippocampal atrophy in the chronic stage (MRI volumetry) (Cerebrovascular Dis.2000;10:2-7.). In the current study with susceptibility-weighted MRI (SWI), we investigated if the delayed T1-hyperintensity in the dorsolateral striatum consistently observed in cardiac arrest survivors represents minor hemorrhage (methemoglobin) or signifies selective neuronal death without bleeding reported as a specific type of ischemic neurodegeneration (Ann Neurol.2003;54:732-47.). Methods: We studied 11 patients in a vegetative state after unexpected out-of-hospital cardiac arrest who were able to undergo multiple brain MRI. We performed SWI to evaluate if the late-onset striatal T1-hyperintensity represents iron accumulation derived from hemoglobin degradation products or not. Results: In the 11 patients, serial MR images demonstrated delayed T1-hyperintesity in the bilateral striatum from one to two weeks after the onset. The SWI study showed no hypointense change in the striatal T1-hyperintensity. Conclusion: The striatal T1-hyperintensity after cardiac arrest seems to correspond to selective neuronal death and glial proliferation with paramagnetic effects but not hemoglobin degradation due to erythrocyte-extravasation.

Post-ischemic gene transfer of IL-10 protects against global brain ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S507-S507 ◽  
Author(s):  
Takashi Shichita ◽  
Hiroaki Ooboshi ◽  
Yasuhiro Kumai ◽  
Masahiro Kumai ◽  
Junichi Takada ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Brain Ischemia ◽  
Global Brain Ischemia ◽  
Global Brain

Platelets apoptosis in rats after global brain ischemia

2018 ◽  
pp. 27-35
Author(s):  
А.А. Соколовская ◽  
Э.Д. Вирюс ◽  
В.В. Александрин ◽  
А.С. Роткина ◽  
К.А. Никифорова ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Ischemic Stroke ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Brain Ischemia ◽  
Mitochondrial Membrane ◽  
Male Rats ◽  
Global Brain Ischemia ◽  
Platelet Apoptosis ◽  
Global Brain

Цель исследования. Ишемические повреждения головного мозга, являются одной из наиболее частой причин инвалидности и смертности во всем мире. Недавно была установлена роль апоптоза тромбоцитов в патофизиологии инсульта, однако его механизмы до сих пор остаются невыясненными. Несмотря на различные экспериментальные модели, направленные на мониторинг апоптоза тромбоцитов, результаты, относительно изучения и выявления апоптоза тромбоцитов при ишемии головного мозга у крыс, весьма немногочисленны. Цель исследования - анализ апоптоза тромбоцитов с помощью метода проточной цитофлуориметрии на модели глобальной ишемии мозга у крыс. Методика. В экспериментах использовано 6 крыс-самцов Вистар в возрасте от 5 до 6 мес., разделенных на 2 группы: интактный контроль (К) и глобальная ишемия головного мозга. Модель глобальной ишемии головного мозга у крыс воспроизводилась путём билатеральной окклюзии общих сонных артерий на фоне гипотензии. Уровень системного артериального давления снижали посредством кровопотери до 40-45 мм рт. ст. Суспензию тромбоцитов крыс получали методом гельфильтрации с использованием сефарозы 2B. Для анализа экстернализации фосфатидилсерина (ФС) тромбоциты крыс инкубировали с Аннексином V-PE в связывающем буфере. Для оценки митохондриального мембранного потенциала (ММП) тромбоциты инкубировали с катионным красителем JC-1. После инкубации образцы немедленно анализировали на проточном цитофлуориметре FACSCalibur (Becton Dickinson, США). Результаты. Согласно полученным данным, экстернализация ФС на тромбоцитах крыс, перенесших инсульт, была значительно выше (53,45 ± 4,21%), чем в контрольной группе крыс (5,27 ± 2,40%). Данный эффект подтверждается выраженной деполяризацией митохондриальных мембран (DYm). После экспериментальной ишемии мозга почти 40% тромбоцитов было деполяризовано. Заключение. Использованный в работе подбор методов и маркеров обеспечивает понимание механизмов апоптоза тромбоцитов как в экспериментальных, так и в клинических условиях. Полученные данные позволяют сделать заключение, что апоптоз тромбоцитов является одним из факторов развития глобальной ишемии головного мозга у крыс. Результаты могут быть использованы для понимания механизмов, участвующих в развитии ишемического повреждения, что, в свою очередь, может быть использовано при разработке новых терапевтических стратегий. Aim. Stroke is one of the most common causes of disability and mortality worldwide. Multiple experimental models of stroke have focused on monitoring of platelet apoptosis. However, studies on and detection of platelet apoptosis in rats with ischemic stroke are very scarce. We investigated platelet apoptosis in rats with global brain ischemia using flow cytometry. Methods. Experiments were carried out on healthy, adult Wistar male rats weighing 300-350 g. The rats were divided into the following 2 groups: intact rats and rats with global brain ischemia. Global brain ischemia was induced by two-vessel (2-VO) carotid occlusion in combination with hypotension. Systemic blood pressure was reduced by 40-45 mm Hg by inducing haemorrhage. Platelets were isolated by gel filtration on Sepharose 2B. For evaluation of phosphatidylserine (PS) externalization, platelets were incubated with Annexin V-PE and analyzed on FACSCalibur (BD Biosciences). Mitochondrial membrane potential (DY) was measured during platelets apoptosis using JC-1, a mitochondrial membrane potential indicator. Platelets were analyzed by flow cytometry immediately after the incubation. Results. PS externalization on platelets was significantly greater after global brain ischemia (53.45 ± 4.21%) than in the control group (5.27 ± 2.40%). Pronounced depolarization of mitochondrial membrane potential (DYm) confirmed this finding. In the rat group with experimental brain ischemia, almost 40% (35.24 ± 5.21%) of platelets were depolarized. Conclusion. Our results provide insight into mechanisms involved in platelet apoptosis during ischemic stroke and can be used in further development of new therapeutic strategies.

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