Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications

J. Marc Simard, Thomas A. Kent, Mingkui Chen, Kirill V. Tarasov, Volodymyr Gerzanich

Research output: Contribution to journalReview article

473 Scopus citations

Abstract

Focal cerebral ischaemia and post-ischaemic reperfusion cause cerebral capillary dysfunction, resulting in oedema formation and haemorrhagic conversion. There are substantial gaps in understanding the pathophysiology, especially regarding early molecular participants. Here, we review physiological and molecular mechanisms involved. We reaffirm the central role of Starling's principle, which states that oedema formation is determined by the driving force and the capillary "permeability pore". We emphasise that the movement of fluids is largely driven without new expenditure of energy by the ischaemic brain. We organise the progressive changes in osmotic and hydrostatic conductivity of abnormal capillaries into three phases: formation of ionic oedema, formation of vasogenic oedema, and catastrophic failure with haemorrhagic conversion. We suggest a new theory suggesting that ischaemia-induced capillary dysfunction can be attributed to de novo synthesis of a specific ensemble of proteins that determine osmotic and hydraulic conductivity in Starling's equation, and whose expression is driven by a distinct transcriptional program.

Original languageEnglish (US)
Pages (from-to)258-268
Number of pages11
JournalLancet Neurology
Volume6
Issue number3
DOIs
StatePublished - Mar 2007

ASJC Scopus subject areas

  • Clinical Neurology

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