Experimental Intracerebral Hemorrhage Effect of Lysed Erythrocytes on Brain Edema and Blood-Brain Barrier Permeability

Bhasin, Rama; Xi, G.; Hua, Ya; Keep, Richard F.; Hoff, Julian T.

doi:10.1007/978-3-7091-6738-0_65

Cited by 26 publications

(26 citation statements)

References 6 publications

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Section: Rbc Lysis Productionmentioning

confidence: 99%

“…All of Hb, heme and iron causes significant brain edema after the first 24 h, which is related to a threefold increase of BBB permeability [44] . Animal experiments showed that intracerebral injection of packed RBCs does not produce significant edema on the first day but does at 3 days; so RBCs can cause delayed brain edema, which results from cellular lysis and BBB disruption by RBCs [44,45] . Brain iron is an erythrocyte degradation product; iron deposition is found in the perihematomal brain tissue during the 1st day after ICH, peaking after 7 days and remaining at a high level for at least 2 weeks, and perihematoma water content increases progressively over course of time [46] .…”

Section: Rbc Lysis Productionmentioning

confidence: 99%

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Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

et al. 2016

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Background: Intracerebral hemorrhage (ICH) is a subtype of stroke with a severe high mortality and disability rate and accounts for about 10-15% of all strokes. The oppression and destruction by hematoma to brain tissue cause the primary brain injury. The inflammation and coagulation response after ICH would accelerate the formation of brain edema around hematoma, resulting in a more severe and durable injury. Currently, treatments for ICH are focusing on the primary injury including reducing intracranial hypertension, blood pressure control, and rehabilitation. There is a short-of-effective medical treatment for secondary inflammation and reducing brain edema in ICH patients. So, it is very important to study on the relationship between brain edema and ICH. Summary: Many molecular and cellular mechanisms contribute to the formation and progress of brain edema after ICH; inhibition of brain edema provides favorable outcome of ICH. Key Messages: This review mainly discusses the pathology and mechanism of brain edema, the effects of brain edema on ICH, and the methods of treating brain edema after ICH.

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Section: Rbc Lysis Productionmentioning

confidence: 99%

Section: Rbc Lysis Productionmentioning

confidence: 99%

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

et al. 2016

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“…The brain was dissected into the cortex, basal ganglia area, and cerebellum. The brain samples were weighed immediately after dissection (wet weight) and then dried at 105°C for 24 h. The percent water content was calculated as [(wet weight Ϫ dry weight)/ wet weight] ϫ 100% as described previously (9).…”

Section: Brain Water Contentmentioning

confidence: 99%

Role of AT₁ receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury

Kusaka¹,

Kusaka²,

Zhou³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

122

102

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jective of the present study was to examine the role of the angiotensin II type 1 receptor (AT1-R) in the diabetes-aggravated oxidative stress and brain injury observed in a rat model of combined diabetes and focal cerebral ischemia. Diabetes was induced by an injection of streptozotoxin (STZ; 55 mg/kg iv) at 8 wk of age. Two weeks after the induction of diabetes, some animals received continuous subcutaneous infusion of the AT1-R antagonist candesartan (0.5 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) for 14 days. Focal cerebral ischemia, induced by middle cerebral artery occlusion/reperfusion (MCAO), was conducted at 4 wk after STZ injection. Male Sprague-Dawley rats (n ϭ 189) were divided into five groups: normal control, diabetes, MCAO, diabetes ϩ MCAO, and diabetes ϩ MCAO ϩ candesartan. The major observations were that 1) MCAO produced typical cerebral infarction and neurological deficits at 24 h that were accompanied by elevation of NAD(P)H oxidase gp91 phox and p22 phox mRNAs, and lipid hydroperoxide production in the ipsilateral hemisphere; 2) diabetes enhanced NAD(P)H oxidase gp91 phox and p22 phox mRNA expression, potentiated lipid peroxidation, aggravated neurological deficits, and enlarged cerebral infarction; and 3) candesartan reduced the expression of gp91 phox and p22 phox , decreased lipid peroxidation, lessened cerebral infarction, and improved the neurological outcome. We conclude that diabetes exaggerates the oxidative stress, NAD(P)H oxidase induction, and brain injury induced by focal cerebral ischemia. The diabetes-aggravated brain injury involves AT1-Rs. We have shown for the first time that candesartan reduces brain injury in a combined model of diabetes and cerebral ischemia.angiotensin type 1 receptor antagonist IT HAS BEEN ESTABLISHED THAT diabetes is a risk factor for cerebral ischemia, and the relative risk of cerebral ischemia in diabetic patients is approximately twice as much as in patients without diabetes (6,15,28). In addition, diabetes is strongly related to early brain injury and to the poor outcome after cerebral ischemia (10,28,54). Clinical studies on diabetic patients showed that hyperglycemia augments brain lesions associated with cerebral ischemia (29,47). In animal models of cerebral ischemia, hyperglycemic animals suffered greater neurological deficit with extensive brain damage and widespread necrosis than nonhyperglycemic animals (17, 53). One of the mechanisms of diabetes-enhanced brain injury is oxidative stress caused by hyperglycemia (58).Reactive oxygen species-mediated oxidative stress is believed to produce tissue injury in wide variety of diseases, including diabetes (58). Several enzymes, especially NAD(P)H oxidase, are recognized as being potentially able to produce reactive oxygen species during diabetes (31). NAD(P)H oxidase consists of five major subunits: a plasma membrane spanning cytochrome b 558 composed of the large subunit gp91 phox , the smaller p22 phox subunit, and three cytosolic compounds (p47 phox , p67 phox , and p40 phox ) (19,30). When cells are stimulated, th...

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“…Red blood cell lysis has been shown to contribute to edema formation after intracerebral hemorrhage at the same time that HO-1 expression and iron accumulation are enhanced, suggesting that heme and its degradation products are associated with breakdown of the blood-brain barrier (Bhasin et al, 2002;Hoff and Xi, 2003;Wu et al, 2003Wu et al, , 2002Xi et al, 2001). Damage to the vascular endothelium may be because of oxidative stress perpetuated by iron (Ogihara et al, 1999;Wu et al, 2003Wu et al, , 2002 and furthermore the administration of iron chelators attenuates edema after intracerebral hemorrhage (Huang et al, 2002).…”

Section: Heme Oxygenase As Modulator Of Neural Injurymentioning

confidence: 99%

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

Chang

Claus

Vreman

et al. 2005

J Cereb Blood Flow Metab

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Intracranial bleeding is one of the most prominent aspects in the clinical diagnosis and prognosis of traumatic brain injury (TBI). Substantial amounts of blood products, such as heme, are released because of traumatic subarachnoid hemorrhages, intraparenchymal contusions, and hematomas. Despite this, surprisingly few studies have directly addressed the role of blood products, in particular heme, in the setting of TBI. Heme is degraded by heme oxygenase (HO) into three highly bioactive products: iron, bilirubin, and carbon monoxide. The HO isozymes, in particular HO-1 and HO-2, exhibit significantly different expression patterns and appear to have specific roles after injury. Developmentally, differences between the adult and immature brain have implications for endogenous protection from oxidative stress. The aim of this paper is to review recent advances in the understanding of heme regulation and metabolism after brain injury and its specific relevance to the developing brain. These findings suggest novel clinical therapeutic options for further translational study.

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Experimental Intracerebral Hemorrhage Effect of Lysed Erythrocytes on Brain Edema and Blood-Brain Barrier Permeability

Cited by 26 publications

References 6 publications

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Role of AT₁ receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

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Experimental Intracerebral Hemorrhage Effect of Lysed Erythrocytes on Brain Edema and Blood-Brain Barrier Permeability

Cited by 26 publications

References 6 publications

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Mechanism and Therapy of Brain Edema after Intracerebral Hemorrhage

Role of AT1 receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury

Heme Regulation in Traumatic Brain Injury: Relevance to the Adult and Developing Brain

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Role of AT₁ receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury