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pubmed-article:15519182pubmed:abstractTextMitogen-activated protein kinases (MAPK) are important intermediates in the signal transduction pathways involved in neuronal dysfunction following cerebral ischemia-reperfusion injury. One subfamily, extracellular regulated kinase 1/2, has been heavily implicated in the pathogenesis of post-ischemic neuronal damage. However, the contribution of extracellular regulated kinase 1/2 to neuronal damage following deep hypothermic circulatory arrest and low flow cardiopulmonary bypass is unknown. We attempted to correlate the extent of neuronal damage present following deep hypothermic circulatory arrest and low flow cardiopulmonary bypass with phosphorylated extracellular regulated kinase 1/2 expression in the cerebral vascular endothelium.lld:pubmed
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pubmed-article:15519182pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:15519182pubmed:articleTitleCerebral activation of mitogen-activated protein kinases after circulatory arrest and low flow cardiopulmonary bypass.lld:pubmed
pubmed-article:15519182pubmed:affiliationDivision of Cardiothoracic Surgery, St Louis University Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis, MO 63110-0250, USA.lld:pubmed
pubmed-article:15519182pubmed:publicationTypeJournal Articlelld:pubmed