Cytotoxic edema: mechanisms of pathological cell swelling

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✓Cerebral edema is caused by a variety of pathological conditions that affect the brain. It is associated with two separate pathophysiological processes with distinct molecular and physiological antecedents: those related to cytotoxic (cellular) edema of neurons and astrocytes, and those related to transcapillary flux of Na+ and other ions, water, and serum macromolecules. In this review, the authors focus exclusively on the first of these two processes. Cytotoxic edema results from unchecked or uncompensated influx of cations, mainly Na+, through cation channels. The authors review the different cation channels that have been implicated in the formation of cytotoxic edema of astrocytes and neurons in different pathological states. A better understanding of these molecular mechanisms holds the promise of improved treatments of cerebral edema and of the secondary injury produced by this pathological process.

Abbreviations used in this paper:ADP = adenosine diphosphate; AQP = aquaporin; ASIC = acidsensing ion channel; ATP = adenosine triphosphate; CNS = central nervous system; CSF = cerebrospinal fluid; MCA = middle cerebral artery; NCCa-ATP = calcium-activated, ATP-sensitive nonselective cation; NKCC = Na+/K+/2Cl-cotransporter; NMDA = N-methyl-D-aspartate; SUR1 = sulfony-lurea receptor 1; TRP = transient receptor potential; TRPC = TRP canonical; TRPM = TRP melastatin; TRPV = TRP vanilloid.

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Address reprint requests to: J. Marc Simard, M.D., Ph.D., University of Maryland Department of Neurological Surgery, 22 South Greene Street, Suite 12SD, Baltimore, Maryland 21201–1595. email: msimard@smail.umaryland.edu.

© AANS, except where prohibited by US copyright law.

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