Complications of intracerebral haemorrhage

Balami, Joyce S.; Buchan, Alastair

doi:10.1016/s1474-4422(11)70264-2

Cited by 376 publications

(294 citation statements)

References 180 publications

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“…5 C. Microglia/macrophages were considered to be CD45 þ CD11b þ . For Foxp3 staining, the CD45-APC-, CD3-Percpcy5.5-, and CD4-PE/cy7-stained cells were fixed, permeabilized using a foxp3 fixed/permeabilization buffer set (Ebioscience), and stained with Foxp3 (1:100, Ebioscience) at 4 C in dark for 20 min.…”

Section: Facs Analysismentioning

confidence: 99%

RETRACTED: Regulatory T cells ameliorate intracerebral hemorrhage-induced inflammatory injury by modulating microglia/macrophage polarization through the IL-10/GSK3β/PTEN axis

Zhou

Zhong

Wang

et al. 2016

J Cereb Blood Flow Metab

162

144

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Inflammation mediated by the peripheral infiltration of inflammatory cells plays an important role in intracerebral hemorrhage (ICH) induced secondary injury. Previous studies have indicated that regulatory T lymphocytes (Tregs) might reduce ICH-induced inflammation, but the precise mechanisms that contribute to ICH-induced inflammatory injury remain unclear. Our results show that the number of Tregs in the brain increases after ICH. Inducing Tregs deletion using a CD25 antibody or Foxp3 DTR -mice increased neurological deficient scores (NDS), the level of inflammatory factors, hematoma volumes, and neuronal degeneration. Meanwhile, boosting Tregs using a CD28 super-agonist antibody reduced the inflammatory injury. Furthermore, Tregs depletion shifted microglia/macrophage polarization toward the M1 phenotype while boosting Tregs shifted this transition toward the M2 phenotype. In vitro, a transwell co-culture model of microglia and Tregs indicated that Tregs changed the polarization of microglia, decreased the expression of MHC-II, IL-6, and TNF-a and increased CD206 expression. IL-10 originating from Tregs mediated the microglia polarization by increasing the expression of Glycogen Synthase Kinase 3 beta (GSK3b), which phosphorylates and inactivates Phosphatase and Tensin homologue (PTEN) in microglia, TGF-b did not participate in this conversion. Thus, Tregs ameliorated ICH-induced inflammatory injury by modulating microglia/macrophage polarization toward the M2 phenotype through the IL-10/GSK3b/PTEN axis.

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Section: Facs Analysismentioning

confidence: 99%

RETRACTED: Regulatory T cells ameliorate intracerebral hemorrhage-induced inflammatory injury by modulating microglia/macrophage polarization through the IL-10/GSK3β/PTEN axis

Zhou

Zhong

Wang

et al. 2016

J Cereb Blood Flow Metab

162

144

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“…9,29 The critical role of glutamate in ICH outcome has led to the use of different types of glutamate antagonists (mainly NMDA antagonist) as potential treatments against hematoma lesions after hemorrhage. In this regard, drugs such as MK801 or memantine have showed positive results in animal models of ICH when hematoma volume and brain edema are analyzed.…”

Section: Discussionmentioning

confidence: 99%

“…29 Although the precise mechanisms involved in the deleterious effect of early hematoma growth during the acute phase are also poorly understood, matrix metalloproteinase overexpression, breakdown of the brain-blood barrier, and intracranial pressure are proposed as important processes associated with early hematoma damage higher than other secondary mechanisms such as glutamate toxicity. 29,35 In fact, glutamate release is transiently accumulated in the perihematoma region due to hematoma expansion, and minimal invasive surgery for removal of intracerebral hematoma and pressure are able to reduce the glutamate content significantly. 36 In this line, we dare to hypothesize that glutamate release could be considered an epiphenomenon of ICH, involved in neuronal damage, although with a less important role than other molecular mechanisms, such as brain-blood barrier breakdown or intracranial pressure.…”

Section: Discussionmentioning

confidence: 99%

Blood Glutamate Grabbing Does Not Reduce the Hematoma in an Intracerebral Hemorrhage Model but it is a Safe Excitotoxic Treatment Modality

Silva‐Candal

Vieites‐Prado

Gutiérrez-Fernández

et al. 2015

J Cereb Blood Flow Metab

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Recent studies have shown that blood glutamate grabbing is an effective strategy to reduce the excitotoxic effect of extracellular glutamate released during ischemic brain injury. The purpose of the study was to investigate the effect of two of the most efficient blood glutamate grabbers (oxaloacetate and recombinant glutamate oxaloacetate transaminase 1: rGOT1) in a rat model of intracerebral hemorrhage (ICH). Intracerebral hemorrhage was produced by injecting collagenase into the basal ganglia. Three treatment groups were developed: a control group treated with saline, a group treated with oxaloacetate, and a final group treated with human rGOT1. Treatments were given 1 hour after hemorrhage. Hematoma volume (analyzed by magnetic resonance imaging (MRI)), neurologic deficit, and blood glutamate and GOT levels were quantified over a period of 14 days after surgery. The results observed showed that the treatments used induced a significant reduction of blood glutamate levels; however, they did not reduce the hematoma, nor did they improve the neurologic deficit. In the present experimental study, we have shown that this novel therapeutic strategy is not effective in case of ICH pathology. More importantly, these findings suggest that blood glutamate grabbers are a safe treatment modality that can be given in cases of suspected ischemic stroke without previous neuroimaging. Keywords: blood glutamate grabbing; GOT; intracerebral hemorrhage; oxaloacetate; protection INTRODUCTION Intracerebral hemorrhage (ICH) represents approximately 15% of all strokes; moreover, the incidence of ICH is expected to grow, given the increase in the use of anticoagulants and aging of the population. Journal of Cerebral Blood1 It is a type of acute stroke characterized by extravasation of blood into the brain parenchyma and formation of hematoma. Hematoma produces primary damage because of the toxic effect of thrombin, a mass effect due to the extravasated blood that compresses the surrounding brain tissue; sometimes, this damage is also enhanced by rebleeding. Primary damage is followed by a secondary damage mainly characterized by edema formation, tissular ischemia, and glutamate excitotoxicity.

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“…6 Neurological complications of sICH -including haematoma expansion, peri-haematomal oedema, intraventricular extension of haemorrhage, hydrocephalus, seizures and non-neurological complications, such as aspiration pneumonia and venous thromboembolism -all lead to poor prognosis. 7,8 Therefore, the aim of acute management is to detect and prevent these complications. Importantly, an early do not attempt resuscitation (DNAR) order should be avoided in the first few days since it limits optimal medical care and results in poor outcome.…”

Section: Acute Medical Managementmentioning

confidence: 99%

Management of acute intracerebral haemorrhage – an update

et al. 2017

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Managing acute intracerebral haemorrhage is a challenging task for physicians. Evidence shows that outcome can be improved with admission to an acute stroke unit and active care, including urgent reversal of anticoagulant effects and, potentially, intensive blood pressure reduction. Nevertheless, many management issues remain controversial, including the use of haemostatic therapy, selection of patients for neurosurgery and neurocritical care, the extent of investigations for underlying causes and the benefi t versus risk of restarting antithrombotic therapy after an episode of intracerebral haemorrhage.

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Complications of intracerebral haemorrhage

Cited by 376 publications

References 180 publications

RETRACTED: Regulatory T cells ameliorate intracerebral hemorrhage-induced inflammatory injury by modulating microglia/macrophage polarization through the IL-10/GSK3β/PTEN axis

RETRACTED: Regulatory T cells ameliorate intracerebral hemorrhage-induced inflammatory injury by modulating microglia/macrophage polarization through the IL-10/GSK3β/PTEN axis

Blood Glutamate Grabbing Does Not Reduce the Hematoma in an Intracerebral Hemorrhage Model but it is a Safe Excitotoxic Treatment Modality

Management of acute intracerebral haemorrhage – an update

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