Background: Gut dysmotility is common after ischemic stroke, but the mechanism underlying this response is unknown. Under homeostasis, gut motility is regulated by the neurons of the enteric nervous system that control contractile/relaxation activity of muscle cells in the gut wall. More recently, studies of gut inflammation revealed interactions of macrophages with enteric neurons are also involved in modulating gut motility.
View Article and Find Full Text PDFTissue injury induced by stroke is traditionally thought to be localised to the brain. However, there is an accumulating body of evidence to demonstrate that stroke promotes pathophysiological consequences in peripheral tissues including the gastrointestinal system. In this study, we investigated the mechanisms underlying gut permeability after stroke.
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