Prevention of disturbances of carbohydrate and oxygen metabolism of the brain and development of cerebral edema by isothiobarbamine in the early period after intracerebral hemorrhage

1988 ◽  
Vol 106 (6) ◽  
pp. 1720-1723 ◽  
Author(s):  
M. B. Plotnikov ◽  
T. M. Plotnikova ◽  
T. V. Yakimova ◽  
A. S. Saratikov
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Edema ◽  
Early Period ◽  
Oxygen Metabolism ◽  
The Brain

scholarly journals Basal Ganglia Herniation into the Fourth Ventricle

1997 ◽  
Vol 24 (1) ◽  
pp. 62-63 ◽  
Author(s):  
Mensura Altumbabic ◽  
Marc R. Del Bigio ◽  
Scott Sutherland
Keyword(s):  
Basal Ganglia ◽  
Intracerebral Hemorrhage ◽  
Fourth Ventricle ◽  
Transtentorial Herniation ◽  
Intracerebral Bleeding ◽  
Rare Phenomenon ◽  
The Brain

ABSTRACT:Background:Transtentorial herniation of large cerebral fragments is a rare phenomenon.Method:Case StudyResults:Examination of the brain of a 35-year-old male showed massive intracerebral hemorrhage resulting in displacement of basal ganglia components into the fourth ventricle.Conclusions:Sufficiently rapid intracerebral bleeding can dissect fragments of cerebrum and displace them long distances across the tentorial opening.

Abstract TP291: Hematoma Retraction and Perihematoma Hypodensity in Neutral Brain Model of Intracerebral Hemorrhage

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Shahram Majidi ◽  
Basit Rahim ◽  
Sarwat I Gilani ◽  
Waqas I Gilani ◽  
Malik M Adil ◽  
...  
Keyword(s):  
Biological Activity ◽  
Intracerebral Hemorrhage ◽  
Ct Scan ◽  
Early Period ◽  
Ct Scans ◽  
Hematoma Expansion ◽  
Human Cadaver ◽  
Fresh Blood ◽  
The Right

Background: The temporal evolution of intracerebral hematomas and perihematoma edema in the ultra-early period on computed tomographic (CT) scans in patients with intracerebral hemorrhage (ICH) is not well understood. We aimed to investigate hematoma and perihematoma changes in “neutral brain” models of ICH. Methods: One human and 6 goat cadaveric heads were used as “neutral brains” to provide physical properties of the brain without any biological activity or new bleeding. ICH was induced by slow injection of 4 ml of fresh blood into the right basal ganglia of the goat brains. Similarly, 20 ml of fresh blood was injected deep into the white matter of the human cadaver head in each hemisphere. Serial CT scans of the heads were performed at 0, 1, 3, and 5 hours after inducing ICH. Analyze software (AnalyzeDirect, Overland Park, KS) was used to measure hematoma and perihematoma hypodensity volumes in the baseline and follow up CT scans. Results: The initial hematoma volumes of 11.6 ml and 10.5 ml in the right and the left hemispheres of the human cadaver brain gradually decreased to 6.6 ml and 5.4 ml at 5 hours, showing 43% and 48% retraction of hematoma, respectively. The volume of the perihematoma hypodensity in the right and left hemisphere increased from 2.6 ml and 2.2 ml in the 1 hour follow up CT scans to 4.9 ml and 4.4 ml in the 5 hour CT scan, respectively. Hematoma retraction was also observed in all six ICH models in the goat brains. The mean ICH volume in the goat heads was decreased from 1.49 ml in the baseline CT scan to 1.01 ml in the 5 hour follow up CT scan showing 29.6% hematoma retraction. Perihematoma hypodensity was visualized in 70% of ICH in goat brains, with an increasing mean hypodensity volume of 0.4 ml in the baseline CT scan to 0.8 ml in the 5 hour follow up CT scan. Conclusion: Our study demonstrated that substantial hematoma retraction and perihematoma hypodensity occurs in intracerebral hematomas in the absence of any new bleeding or biological activity of the surrounding brain. Such observations suggest that active bleeding is underestimated in patients with no or small hematoma expansion and our understanding of perihematoma hypodesity needs to be reconsidered.

scholarly journals MSC Secretome as a Promising Tool for Neuroprotection and Neuroregeneration in a Model of Intracerebral Hemorrhage

Pharmaceutics ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2031
Author(s):  
Maxim Karagyaur ◽  
Stalik Dzhauari ◽  
Nataliya Basalova ◽  
Natalia Aleksandrushkina ◽  
Georgy Sagaradze ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Neurological Outcome ◽  
Multipotent Mesenchymal Stromal Cells ◽  
Lesion Volume ◽  
Therapeutic Approaches ◽  
Beneficial Effects ◽  
Tissue Repair And Regeneration ◽  
Promising Tool ◽  
Neurologic Disorders ◽  
The Brain

Multipotent mesenchymal stromal cells (MSCs) are considered to be critical contributors to injured tissue repair and regeneration, and MSC-based therapeutic approaches have been applied to many peripheral and central neurologic disorders. It has been demonstrated that the beneficial effects of MSC are mainly mediated by the components of their secretome. In the current study, we have explored the neuroprotective potential of the MSC secretome in a rat model of intracerebral hemorrhage and shown that a 10-fold concentrated secretome of human MSC and its combination with the brain-derived neurotrophic factor (BDNF) provided a better survival and neurological outcome of rats within 14 days of intracerebral hemorrhage compared to the negative (non-treated) and positive (BDNF) control groups. We found that it was due to the ability of MSC secretome to stimulate neuron survival under conditions of glutamate-induced neurotoxicity. However, the lesion volume did not shrink in these rats, and this also correlated with prominent microglia activation. We hypothesize that this could be caused by the species-specificity of the used MSC secretome and provide evidence to confirm this. Thus, we have found that allogenic rat MSC secretome was more effective than xenogenic human MSC secretome in the rat intracerebral hemorrhage model: it reduced the volume of the lesion and promoted excellent survival and neurological outcome of the treated rats.

scholarly journals Cerebral Edema Formation After Stroke: Emphasis on Blood–Brain Barrier and the Lymphatic Drainage System of the Brain

2021 ◽  
Vol 15 ◽  
Author(s):  
Sichao Chen ◽  
Linqian Shao ◽  
Li Ma
Keyword(s):  
Blood Brain Barrier ◽  
Cerebral Edema ◽  
Lymphatic System ◽  
Vasogenic Edema ◽  
Lymphatic Vessels ◽  
Drainage System ◽  
Brain Barrier ◽  
Edema Formation ◽  
Blood Brain ◽  
The Brain

Brain edema is a severe stroke complication that is associated with prolonged hospitalization and poor outcomes. Swollen tissues in the brain compromise cerebral perfusion and may also result in transtentorial herniation. As a physical and biochemical barrier between the peripheral circulation and the central nervous system (CNS), the blood–brain barrier (BBB) plays a vital role in maintaining the stable microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the dysfunction of the BBB results in increased paracellular permeability, directly contributing to the extravasation of blood components into the brain and causing cerebral vasogenic edema. Recent studies have led to the discovery of the glymphatic system and meningeal lymphatic vessels, which provide a channel for cerebrospinal fluid (CSF) to enter the brain and drain to nearby lymph nodes and communicate with the peripheral immune system, modulating immune surveillance and brain responses. A deeper understanding of the function of the cerebral lymphatic system calls into question the known mechanisms of cerebral edema after stroke. In this review, we first discuss how BBB disruption after stroke can cause or contribute to cerebral edema from the perspective of molecular and cellular pathophysiology. Finally, we discuss how the cerebral lymphatic system participates in the formation of cerebral edema after stroke and summarize the pathophysiological process of cerebral edema formation after stroke from the two directions of the BBB and cerebral lymphatic system.

scholarly journals Leukocyte dynamics after intracerebral hemorrhage in a living patient reveal rapid adaptations to tissue milieu

2020 ◽  
Author(s):  
Brittany A. Goods ◽  
Michael H. Askenase ◽  
Erica Markarian ◽  
Hannah E. Beatty ◽  
Riley Drake ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Single Cell ◽  
Brain Tissue ◽  
Cellular Response ◽  
Tissue Injury ◽  
Brain Inflammation ◽  
Therapeutic Interventions ◽  
Acute Injury ◽  
The Brain ◽  
Over Time

ABSTRACTIntracerebral hemorrhage (ICH) is a devastating form of stroke with a high mortality rate and few treatment options. Discovery of therapeutic interventions has been slow given the challenges associated with studying acute injury, particularly over time, in the human brain. Inflammation induced by exposure of brain tissue to blood appears to be a major part of brain tissue injury. Here we longitudinally profiled blood and cerebral hematoma effluent from a patient enrolled in the Minimally Invasive Surgery with Thrombolysis in Intracerebral Haemorrhage Evacuation (MISTIEIII) trial, offering a rare window into the local and systemic immune responses to acute brain injury. Using single-cell RNA-sequencing, we characterized the local cellular response during ICH in the brain of a living patient at single-cell resolution for the first time. Our analysis revealed rapid shifts in the activation states of myeloid and T cells in the brain over time, suggesting that leukocyte responses are dynamically reshaped by the hematoma microenvironment. Interestingly, the patient had an asymptomatic re-bleed (second local exposure to blood) that our transcriptional data indicated occurred more than 30 hours prior to detection by CT scan. This case highlights the rapid immune dynamics in the brain after ICH and suggests that sensitive methods like scRNA-seq can inform our understanding of complex intracerebral events.

Effect of ethomersol on blood supply and oxygen metabolism of the brain during acute transient ischemia and recirculation

1991 ◽  
Vol 111 (4) ◽  
pp. 493-495 ◽  
Author(s):  
T. M. Plotnikova ◽  
Z. V. Kulakova ◽  
M. B. Plotnikov
Keyword(s):  
Blood Supply ◽  
Oxygen Metabolism ◽  
Transient Ischemia ◽  
The Brain

scholarly journals 15O Radioactivity Clearance is Faster after Intracarotid Bolus Injection of 15O-Labeled Oxyhemoglobin than after 15O-Water Injection

2003 ◽  
Vol 23 (7) ◽  
pp. 838-844 ◽  
Author(s):  
Chie Seki ◽  
Jeff Kershaw ◽  
Paule-Joanne Toussaint ◽  
Kenichi Kashikura ◽  
Tetsuya Matsuura ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Bolus Injection ◽  
Water Injection ◽  
Oxygen Metabolism ◽  
Blood Stream ◽  
Time Range ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Finite Period ◽  
The Brain

The authors tested the hypothesis that the oxygen content of brain tissue is negligible by injecting an intracarotid bolus of 15O-labeled tracer into rats. Under the hypothesis, the clearance rates of 15O radioactivity from the brain after injections of both 15O-labeled water (H215O) and 15O-labeled oxyhemoglobin (HbO15O) should be identical. However, the logarithmic slope of the 15O radioactivity curve after HbO15O injection (0.494 ± 0.071 min-1) was steeper than that after H215O injection (0.406 ± 0.038 min−1) ( P<0.001, n = 13), where the time range used in the comparison was between 60 and 120 seconds after the injection. A possible interpretation of this result is that nonmetabolized O15O may dwell in the brain tissue for a finite period of time before it is eventually metabolized or returned to the blood stream unaltered. These findings contradict assumptions made by models currently used to measure cerebral oxygen metabolism.

scholarly journals Butin attenuates brain edema in a rat model of intracerebral hemorrhage by anti inflammatory pathway

2018 ◽  
Vol 9 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Peiyu Li ◽  
Cheng Jiwu
Keyword(s):  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Treated Group ◽  
Control Group ◽  
Lesion Volume ◽  
Dependent Manner ◽  
Neurological Score ◽  
Factor Α ◽  
The Brain ◽  
Brain Tissues

Abstract Background This study evaluates the effect of butin against brain edema in intracerebral hemorrhage (ICH). Methodology ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25 and 50 mg/kg group receives butin (25 and 50 mg/kg, i.p.)60 min after the induction of ICH in all animals. One day after neurological score, hemorrhagic injury and expressions of protein responsible for apoptosis and inflammatory cytokines were assessed in the brain tissue of ICH rats. Result Neurological scoring significantly increased and hemorrhagic lesion volume decreased in butin treated group of rats compared to ICH group. However, treatment with butin significantly decreases the ratio of Bax/Bcl-2 and protein expression of Cleaved caspase-3 than ICH group in dose dependent manner. Level of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) in the brain tissues were significantly decreased in the butin treated group than ICH group. In addition butin attenuates the altered signaling pathway of NF-κB in the brain tissues of ICH rats. Conclusion Our study concludes that butin attenuates the altered behavior and neuronal condition in ICH rats by reducing apoptosis and inflammatory response.

Abstract TMP82: Increased Intracerebral Hemorrhage During Acute and Chronic Hypertension in Alzheimer's Transgenic Mice

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
David H Cribbs ◽  
Giselle Passos ◽  
Vitaly Vasilevko
Keyword(s):  
Risk Factor ◽  
Transgenic Mice ◽  
Intracerebral Hemorrhage ◽  
Amyloid Precursor Protein ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Chronic Hypertension ◽  
Cerebrovascular System ◽  
The Brain ◽  
Tg2576 Mice

Hypertension is a major risk factor for intracerebral hemorrhage (ICH), and the accumulation of amyloid-beta (Aβ) in the cerebrovascular system, cerebral amyloid angiopathy (CAA), is also a significant risk factor for intracerebral hemorrhage ICH. Currently, there are no animal studies demonstrating a direct involvement of hypertension in the accumulation of Alzheimer’s disease-like pathology. To address this issue we have developed several mouse models that combine hypertension protocols with amyloid precursor protein (APP) transgenic mice (Tg2576), which accumulate significant CAA in the large cerebral vessels and the meninges by 18 months of age. The goal of this study was to determine the effect of acute and chronic hypertension on ICH in wildtype and a transgenic mouse model overexpressing a mutant human amyloid precursor protein (Tg2576 mice) associated with early onset AD and CAA. Fifteen-month-old Tg2576 mice and non-transgenic (nTg) littermates were treated with an angiotensin II (AngII) infusion (1000 ng/kg/min) and L-NAME (100 mg/kg/day) in drinking water to produce chronic hypertension. One week later, transient acute hypertension was induced by daily AngII injections (0.5 μg/g, s.c., twice daily) to produce ICH. A similar increase in mean blood pressure was observed in Tg2576 and nTg mice when evaluated 2 weeks after initiation of treatment. However Tg2576 mice had a higher incidence of signs of stroke compared with nTg littermates (P > 0.05). These data suggest that the accumulation of Aβ in the brain has an important role in development of ICH. Moreover, there was robust glial activation and increase in CAA in the gray matter of Tg2576 mice showing that hypertension may affect gray as well as white matter in the brain. Further studies may provide insights into the hypertension-induced changes in the cerebral vascular system that initiated the increase in CAA. The accumulation of Aβ in the cerebrovascular system is a significant risk factor for intracerebral hemorrhage (ICH), and has been linked to endothelial transport failure and blockage of perivascular drainage. While management of hypertension and atherosclerosis can reduce the incidence of ICH, there are currently no approved therapies for attenuating CAA.

Abstract P790: Landiolol Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest in Mice

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Tomoyuki Iwai ◽  
Shin Nakayama
Keyword(s):  
Cardiac Arrest ◽  
Water Content ◽  
Cerebral Edema ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
P Value ◽  
Brain Water Content ◽  
Arterial Blood ◽  
The Brain ◽  
Brain Water

Introduction: Cerebral edema following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) is associated with unfavorable neurologic outcome. The Na + -K + -2Cl - water cotransporter NKCC1 is suspected to be a critical mediator of edema formation after ischemia. It is reported that β1 adrenoreceptor antagonists protect neurons following brain ischemia in rodents. β1 adrenoreceptor antagonists inhibit the Na + -K + -ATPase, which can inhibit driving force of NKCC1 that theoretically reduces cerebral edema following ischemia-reperfusion injury. In this study, we examined whether landiolol, a selective β1 adrenoreceptor antagonist, attenuates cerebral edema following CA/CPR. Methods: Isoflurane-anesthetized adult male mice (C57BL/6J, 25-30g) were randomized into landiolol group or control group. After 7-min CA followed by CPR, landiolol (0.5ml, 830μg/ml) was administered by continuous infusion intravenously for 4 hours. Animals in control group were given normal saline (0.5ml) in the same manner. Twenty-four hours after CA/CPR, the brain was removed to assess brain water content using wet-to-dry method. The primary outcome was measurement of the brain water content. Heart rate and arterial blood pressure were recorded. Measured parameters were analyzed by one-way ANOVA with post hoc Tukey-Kramer test using SPSS® statistics 25. Differences were considered statistically significant at a P value < 0.05. Results: Brain water contents was increased in control group mice after CA/CPR (n=10) compared with those in sham operated mice (n=5) (79.5±0.85% vs 78.3±0.14%, P=0.003). Compared with control group, landiolol treatment significantly reduced brain water content in mice subjected to CA/CPR (n=12) (78.9±0.51% vs 79.5±0.85%, P=0.04). Conclusion: Landiolol attenuated brain edema following CA/CPR. These results may suggest selective β1-blocker could be alternative treatment for neuroprotection in patients who suffered CA/CPR.

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