Cytotoxic and Vasogenic Brain Edema

Keep, Richard F.; Andjelkovic, Anuska V.; Xi, G.

doi:10.1016/b978-0-12-803058-5.00029-1

Cited by 13 publications

(15 citation statements)

References 10 publications

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“…Head injury is the leading cause of accident-related death for people under the age of 40 years. Every year approximately 10 million people are hospitalized due to head injuries worldwide [ [25] , [26] , [27] ].…”

Section: Discussionmentioning

confidence: 99%

Effects of caffeic acid phenethyl ester in reducing cerebral edema in rat subjects experiencing brain injury: An in vivo study

Nasution¹,

Islam

Hatta

et al. 2020

Annals of Medicine and Surgery

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Background A head injury is a very dangerous condition that threatens human life. This study examines the use of caffeic acid phenethyl ester (CAPE) in reducing cerebral edema in cases of head injury. The purpose of this study is to demonstrate whether CAPE can improve various parameters related to the expression of Aquaporin-4 (AQP4) mRNA and the serum AQP4 levels in rat subjects. Methods This is a randomized controlled study using a posttest-only control group design that uses experimental animals—specifically, male Rattus norvegicus ( Sprague Dawley strain) rats aged 10–12 weeks and weighing 200–300 g. This study used a head injury model according to Marmarou (1994) with minor modifications to the animal model fixation tool. The parameters of the AQP4 mRNA were examined with real-time PCR, while serum AQP4 levels were examined with sandwich ELISA. Results The AQP4 mRNA expression in rats that were given CAPE was lower than those not given CAPE, both on the fourth and seventh days; serum AQP4 levels in rats that were given CAPE were also lower than those not given CAPE, both on the fourth and seventh days. Conclusion Administration of CAPE in a rat model with head injury can reduce cerebral edema, mediated by AQP4.

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Section: Discussionmentioning

confidence: 99%

Effects of caffeic acid phenethyl ester in reducing cerebral edema in rat subjects experiencing brain injury: An in vivo study

Nasution¹,

Islam

Hatta

et al. 2020

Annals of Medicine and Surgery

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“…The aim was to investigate the cause-and-effect relationship between the trauma model used and the biochemical processes in the blood. Table 1 shows an increase in each indicator—evidenced by the chemical and inflammatory processes—recorded after the head injury [ 5 ]. These results also indicated a secondary brain injury process, due to the trauma model performed on the mice [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…TBI triggers several pathological processes in the brain shortly after trauma. This causes a direct mechanical disruption of brain tissue, along with an indirect mechanism [ 3 ] due to an acute inflammatory response, including: damage to the blood-brain barrier (BBB) [ 4 ]; edema formation; peripheral blood cell infiltration and activation of cell immunocompetence; and intrathecal release from many inflammatory mediators, such as interleukins and chemotactic factors [ 3 , 5 ]. Various mediators involved in forming or exacerbating these pathological processes have been identified [ 5 ], including VEGF (vascular endothelial growth factor), arachidonic acid, bradykinin [ 6 ], Ca2+, glutamate, and free radical oxygen, among others [ 3 , [5] , [6] , [7] ].…”

Section: Introductionmentioning

confidence: 99%

Modification of the Marmarou model in developing countries

Nasution

Islam

Hatta

et al. 2020

Annals of Medicine and Surgery

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Introduction Head injury is an injury or wound of the brain tissue due to external forces; it can cause a decrease or change in the status of consciousness. Many head injury models have used mice as experimental animals; the Marmarou model is the most famous and the most widely-used diffuse brain injury model. In this study, we slightly modified the Marmarou model. The purpose of this study is to help researchers examining head injuries in mice, especially those in developing countries who have limited facilities and infrastructure. Methods This experimental research uses animals models ( Rattus novergicus , strain Sprague Dawley) that fit several criteria, including male, aged 10–12 weeks, and body weight of 200–300 g. This study involves a slight modification on the tube used, with a 20 cm-long weight of 20 g. The blood samples for the following assays of ELISA and brain tissue samples were collected at 24 h and 4, 5, 6, and 7 days post-trauma. Results A significant effect on the brain was seen with the Marmarou model modification, at a mass weight of 20 g and height of 20 cm, with 0.04 J energy produced. Changes were also seen in the histological features of brain tissue and the serum levels of AQP-4, F2 IsoPs, MPO, and VEGF from 24 h until 7 days after trauma. Conclusion This report describes the development of an experimental head injury approach modifying the Marmarou model that is able to produce a diffuse brain injury model in mice.

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“…This is then accompanied by osmotic influx of water into cells, and various ion and water channels have been implicated in this process (e.g., aquaporin-4, Na-K-Cl co-transporter, and sulfonylurea 1 transient receptor potential melastatin 4 (Sur1-Trpm4)) [ 2 , 10 , 11 ]. Cytotoxic edema is driven by ionic dyshomeostasis, and worsens injury by further aggravating ionic dyshomeostasis, cell swelling, and blood-brain barrier (BBB) damage [ 2 , 10 – 13 ]. This then culminates in worsened vasogenic edema [ 2 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…In our first experiment, we hypothesized glibenclamide would not affect cerebral bleeding caused by collagenase, or other safety measures (e.g., blood glucose) at 24 hours [ 29 , 33 ]. In experiment 2, we hypothesized glibenclamide would reduce edema and improve related factors, including BBB integrity and element dyshomeostasis at 24 hours [ 2 , 10 , 11 , 13 ]. Two different stroke severities were administered, deemed to be moderate and severe, to further investigate the effect of glibenclamide in relation to insult severity.…”

Section: Introductionmentioning

confidence: 99%

Glibenclamide does not improve outcome following severe collagenase-induced intracerebral hemorrhage in rats

et al. 2021

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Intracerebral hemorrhage (ICH) is a devastating insult with few effective treatments. Edema and raised intracranial pressure contribute to poor outcome after ICH. Glibenclamide blocks the sulfonylurea 1 transient receptor potential melastatin 4 (Sur1-Trpm4) channel implicated in edema formation. While glibenclamide has been found to improve outcome and reduce mortality in animal models of severe ischemic stroke, in ICH the effects are less clear. In our previous study, we found no benefit after a moderate-sized bleed, while others have reported benefit. Here we tested the hypothesis that glibenclamide may only be effective in severe ICH, where edema is an important contributor to outcome. Glibenclamide (10 μg/kg loading dose, 200 ng/h continuous infusion) was administered 2 hours post-ICH induced by collagenase injection into the striatum of adult rats. A survival period of 24 hours was maintained for experiments 1–3, and 72 hours for experiment 4. Glibenclamide did not affect hematoma volume (~81 μL) or other safety endpoints (e.g., glucose levels), suggesting the drug is safe. However, glibenclamide did not lessen striatal edema (~83% brain water content), ionic dyshomeostasis (Na+, K+), or functional impairment (e.g., neurological deficits (median = 10 out of 14), etc.) at 24 hours. It also did not affect edema at 72 h (~86% brain water content), or overall mortality rates (25% and 29.4% overall in vehicle vs. glibenclamide-treated severe strokes). Furthermore, glibenclamide appears to worsen cytotoxic edema in the peri-hematoma region (cell bodies were 46% larger at 24 h, p = 0.0017), but no effect on cell volume or density was noted elsewhere. Overall, these findings refute our hypothesis, as glibenclamide produced no favorable effects following severe ICH.

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Cytotoxic and Vasogenic Brain Edema

Cited by 13 publications

References 10 publications

Effects of caffeic acid phenethyl ester in reducing cerebral edema in rat subjects experiencing brain injury: An in vivo study

Effects of caffeic acid phenethyl ester in reducing cerebral edema in rat subjects experiencing brain injury: An in vivo study

Modification of the Marmarou model in developing countries

Glibenclamide does not improve outcome following severe collagenase-induced intracerebral hemorrhage in rats

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