2019
DOI: 10.1007/s10072-019-03739-0
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Intestinal barrier dysfunction following traumatic brain injury

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Cited by 37 publications
(26 citation statements)
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“…After the central nervous system is damaged, various pathways in the brain-gut axis are blocked, and many brain-gut peptides are secreted abnormally. These pathways and peptides cannot transmit information normally or stimulate gastrointestinal motility [11][12][13]. The gastrointestinal mucosa is in a state of hypoperfusion, resulting in the spread of focal small ulcers, which usually manifests as stress ulcers.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…After the central nervous system is damaged, various pathways in the brain-gut axis are blocked, and many brain-gut peptides are secreted abnormally. These pathways and peptides cannot transmit information normally or stimulate gastrointestinal motility [11][12][13]. The gastrointestinal mucosa is in a state of hypoperfusion, resulting in the spread of focal small ulcers, which usually manifests as stress ulcers.…”
Section: Discussionmentioning
confidence: 99%
“…The incidence of secondary gastrointestinal dysfunction increased with injury severity, and the GIF score on the rst day and the mean GIF score for the rst three days were signi cantly different among the severe, moderate and mild groups. The intestinal mucosa morphology was found to change within a short time after trauma, including epithelial cell detachment and apoptosis, rupture of the villi, edema of interstitial tissue and the lamina propria, interruption of tight junctions, etc., and the mucosal barrier was observed to have lost its protective function [11]. Additionally, the intestinal ora was completely disordered within a few hours after injury, and the microbial composition and relative abundance changed signi cantly.…”
Section: Discussionmentioning
confidence: 99%
“…The causes of these ndings were analyzed. It was found that the intestinal mucosa morphology had changed within a short time after trauma, including epithelial cell detachment and apoptosis, rupture of the villi, edema of interstitial tissue and the lamina propria, interruption of tight junctions, etc., and that the mucosal barrier had lost its protective function [11] . Additionally, the intestinal ora was completely disordered within a few hours after injury, and the microbial composition and relative abundance changed signi cantly.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, the hemorrhagic shock is associated with barrier dysfunction of the gut and development of MODS after the trauma and can lead to a traumatic endotheliopathy by glycocalyx degradation, like in the CNS [50]. Studies have shown that paracellular hyperpermeability due to inflammatory reactions and abnormal release of neurotransmitters is the basis for intestinal barrier dysfunction after TBI [51]. The increased permeability of the organ barriers allows metabolites to enter the bloodstream and to detect specific biomarkers [14].…”
Section: Severe Traumatic Brain Injury (Tbi) Modulates Kinetic Profilmentioning
confidence: 99%