Why the study?
Acute lung injury is a common complication after THS/R, and this study aimed to explore the effects of vagus nerve stimulation on intestinal epithelial glycocalyx and acute lung injury associated with THS/R.
Does vagus nerve stimulation reduce acute lung injury and intestinal epithelial glycocalyx damage in a rat model of traumatic hemorrhagic shock/resuscitation?
Does vagus nerve stimulation reduce acute lung injury and intestinal epithelial glycocalyx damage in a rat model of traumatic hemorrhagic shock/resuscitation?
Vagus nerve stimulation mitigates acute lung injury following traumatic hemorrhagic shock/resuscitation by protecting the intestinal epithelial glycocalyx via the cholinergic anti-inflammatory pathway.
VNS may protect glycocalyx and reduce ALI in rat THS/R models; leaves open clinical translation.
BackgroundAcute lung injury (ALI) is a common complication after THS/R, and vagus nerve stimulation (VNS) could alleviate lung injury by activating cholinergic anti-inflammatory pathway (CAP) during traumatic hemorrhagic shock/resuscitation (THS/R). The purpose of this study was to explore the effects of VNS on intestinal epithelial glycocalyx and acute lung injury associated with THS/R.MethodsSprague-Dawley rats were subjected to traumatic hemorrhagic shock/ resuscitation to induce ALI. The measurements of intestinal barrier permeability, intestinal epithelial glycocalyx, and the level of inflammation factors and histology of lung and gut tissue were made in each group.ResultsThe level of TNF-α,IL-6 and MPO in lung and gut tissue were significantly decreased in the VNS-treated group. In addition, the shedding of intestinal epithelial glycocalyx and increased gut barrier permeability were alleviated in the VNS-treated group, and the gut tissue and lung tissue injury were mitigated in the VNS-treated group. However, pretreated with methyllycaconitine could reverse the protective effect of VNS.ConclusionsVNS could relieve lung injury associated with THS/R by alleviating the damage of intestinal epithelial glycocalyx, which might be achieved by activating CAP.
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Wu et al. (2020) studied this question.
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