Pathophysiological aspects of brain edema

Go, K.G.

doi:10.1016/0303-8467(84)90069-6

Cited by 8 publications

(2 citation statements)

References 21 publications

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“…The pathophysiological swelling of brain tissue is a main feature of cerebral edema due to the progressive increase in water content [9]. A logical explanation to understanding the mechanisms of cerebral edema formation was first carried out by Igor Klatzo, where he classified edema into cytotoxic and vasogenic types [10]; a third type, named hydrocephalic edema or interstitial edema, has subsequently been described [11].…”

Section: Brain Edemamentioning

confidence: 99%

Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Tang

Yang

2016

IJMS

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Aquaporin-4 (AQP4) is a family member of water-channel proteins and is dominantly expressed in the foot process of glial cells surrounding capillaries. The predominant expression at the boundaries between cerebral parenchyma and major fluid compartments suggests the function of aquaporin-4 in water transfer into and out of the brain parenchyma. Accumulating evidences have suggested that the dysregulation of aquaporin-4 relates to the brain edema resulting from a variety of neuro-disorders, such as ischemic or hemorrhagic stroke, trauma, etc. During edema formation in the brain, aquaporin-4 has been shown to contribute to the astrocytic swelling, while in the resolution phase, it has been seen to facilitate the reabsorption of extracellular fluid. In addition, aquaporin-4-deficient mice are protected from cytotoxic edema produced by water intoxication and brain ischemia. However, aquaporin-4 deletion exacerbates vasogenic edema in the brain of different pathological disorders. Recently, our published data showed that the upregulation of aquaporin-4 in astrocytes probably contributes to the transition from cytotoxic edema to vasogenic edema. In this review, apart from the traditional knowledge, we also introduce our latest findings about the effects of mesenchymal stem cells (MSCs) and microRNA-29b on aquaporin-4, which could provide powerful intervention tools targeting aquaporin-4.

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Section: Brain Edemamentioning

confidence: 99%

Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Tang

Yang

2016

IJMS

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“…A case in point is the critical role of the glymphatic system in understanding the occurrence of brain edema. Traditionally, brain edema is thought to be formed entirely by fluid accumulation in the intravascular compartment ( Go, 1984 ). However, relevant studies of the glymphatic system have found that CSF is the primary source of initial brain edema rather than blood leakage ( Mestre et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

The glymphatic system: a new perspective on brain diseases

Zhao

Fan

Zhang

et al. 2023

Front. Aging Neurosci.

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The glymphatic system is a brain-wide perivascular pathway driven by aquaporin-4 on the endfeet of astrocytes, which can deliver nutrients and active substances to the brain parenchyma through periarterial cerebrospinal fluid (CSF) influx pathway and remove metabolic wastes through perivenous clearance routes. This paper summarizes the composition, overall fluid flow, solute transport, related diseases, affecting factors, and preclinical research methods of the glymphatic system. In doing so, we aim to provide direction and reference for more relevant researchers in the future.

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Nuclear magnetic resonance relaxation in experimental brain edema: Effects of water concentration, protein concentration, and temperature

Kamman

Brouwer

et al. 1988

Magnetic Resonance in Med

109

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Proton relaxation times T1 and T2 of macromolecular solutions, bovine brain tissues, and experimental cat brain edema tissues were studied as a function of water concentration, protein concentration, and temperature. A linear relation was found between the inverse of the weight fraction of tissue water and the spin-lattice relaxation rate, R1, based on a fast proton exchange model for relaxation. This correlation was also found for the spin-spin relaxation rate, R2, of gray matter samples and macromolecular solutions at low concentrations. Concentrated solutions of protein-water samples showed an enhanced relaxation due to viscosity effects. The T2 of white matter was considerably lengthened with elevated water concentration, but showed no straightforward relation with the total tissue water content. The relaxation times of all samples increased with temperature, supporting the assumption of fast proton exchange in the model for relaxation. This was not found for white matter, in which T2 decreased with increasing temperature, which indicated that intermediate or even slow exchange was present. The relation found between relaxation times and tissue water content can be used to predict the amount of and/or increase in tissue water due to water-elevating processes such as edema.

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Pathophysiological aspects of brain edema

Cited by 8 publications

References 21 publications

Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

Aquaporin-4: A Potential Therapeutic Target for Cerebral Edema

The glymphatic system: a new perspective on brain diseases

Nuclear magnetic resonance relaxation in experimental brain edema: Effects of water concentration, protein concentration, and temperature

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