2013
DOI: 10.1097/shk.0b013e31828def5a
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Parasympathetic Stimulation Via the Vagus Nerve Prevents Systemic Organ Dysfunction by Abrogating Gut Injury and Lymph Toxicity in Trauma and Hemorrhagic Shock

Abstract: JW: Pretreatment with high-fat enteral nutrition reduces endotoxin and TNF-a and preserves gut barrier function early after hemorrhagic shock. Shock 21(1):65Y71, 2004. 6. Luyer MD, Buurman WA, Hadfoune M, Wolfs T, van't Veer C, Jacobs JA, Dejong CH, Greve JW: Exposure to bacterial DNA before hemorrhagic shock strongly aggravates systemic inflammation and gut barrier loss via an IFNgammaYdependent route. Ann Surg 245(5):795Y802, 2007. 7. Lubbers T, Luyer MD, de Haan JJ, Hadfoune M, Buurman WA, Greve JW: Lipid-r… Show more

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Cited by 8 publications
(6 citation statements)
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“…A previous study demonstrated that activation of ɑ7nAChR could improve POCD via vagal anti-inflammatory reflex [ 65 ]. It was also reported that the vagal anti-inflammatory reflex could be activated by enteral administration of boluses of lipid and protein enriched nutrition [ 66 , 67 ]. These nutrients were capable of stimulating cholecystokinin (CCK)-mediated CCK-1 receptor in the gut to activate the vagal afferent nerves and subsequently inhibit proinflammatory cytokine release via nicotinergic acetylcholine receptors [ 67 , 68 ].…”
Section: Introductionmentioning
confidence: 99%
“…A previous study demonstrated that activation of ɑ7nAChR could improve POCD via vagal anti-inflammatory reflex [ 65 ]. It was also reported that the vagal anti-inflammatory reflex could be activated by enteral administration of boluses of lipid and protein enriched nutrition [ 66 , 67 ]. These nutrients were capable of stimulating cholecystokinin (CCK)-mediated CCK-1 receptor in the gut to activate the vagal afferent nerves and subsequently inhibit proinflammatory cytokine release via nicotinergic acetylcholine receptors [ 67 , 68 ].…”
Section: Introductionmentioning
confidence: 99%
“…CART was also described within the enteric nervous system (ENS), which, apart from extrinsic sympathetic and parasympathetic innervation of the gastrointestinal (GI) tract , Luyer et al 2013, plays a crucial role in the control of all intestinal functions. The ENS comprises of millions of neurons, and its construction depends on the segment of GI tract and animal species.…”
Section: Introductionmentioning
confidence: 99%
“…The vagal anti-inflammatory reflex ( Tracey, 2002 , 2007 ) contributes to the regulation (inhibition/termination) of inflammatory responses. In different animal models ( de Haan et al., 2010a , de Haan et al., 2010b ; de Haan et al., 2010a , de Haan et al., 2010b ; de Haan et al., 2013 ; Lubbers et al., 2010a , Lubbers et al., 2010b , Lubbers et al., 2010c ; Lubbers et al., 2010a , Lubbers et al., 2010b , Lubbers et al., 2010c ; Luyer et al., 2013 ), activation of this reflex by lipid-enriched nutrition inhibited the response on inflammatory stimuli. These effects were abrogated by vagotomy, CCK-1 receptor antagonists or nicotinergic acetylcholine receptor antagonists ( Lubbers et al., 2010 ; Matteoli and Boeckxstaens, 2013 ).…”
Section: Discussionmentioning
confidence: 99%
“…These nutrients stimulated cholecystokinin (CCK)-mediated CCK-1 receptors in the gut, thereby activating the afferent vagal nerves. Consequently, vagal efferent nerves in the central nervous system are stimulated, resulting in inhibition of the release of pro-inflammatory cytokines via nicotinergic acetylcholine receptors ( de Haan et al., 2010 ; de Haan et al., 2010a , de Haan et al., 2010b ; de Haan et al., 2014 ; Lubbers et al., 2010a , Lubbers et al., 2010b , Lubbers et al., 2010c ; Luyer et al., 2013 ). In mice, lipid-rich nutrition before Lipopolysaccharide (LPS) administration attenuated the inflammatory response and intestinal damage through the nutritional vagal anti-inflammatory pathway ( Lubbers et al., 2010 ).…”
Section: Introductionmentioning
confidence: 99%