Activation of vagovagal reflex prevents hepatic ischaemia-reperfusion-induced lung injury via anti-inflammatory and antioxidant effects.

New findings What is the central question of this study? Does VNS have protective effects against both direct liver damage and distant lung injury in a hepatic ischemia/reperfusion rat model? What is the main finding and its importance? VNS provides the protective effects through anti-inflammation and anti-oxidative stress possibly achieved by the vagovagal reflex. Abstract Hepatic ischemia reperfusion (I/R) is not an isolated event; instead, it can result in remote organ dysfunction. The aim of this study was to investigate whether vagal nerve stimulation (VNS) can alleviate hepatic I/R-induced lung injury and to explore the underlying mechanism. Thirty male Sprague-Dawley rats were randomly allocated into five groups (n = 6 each): the sham group (without I/R or VNS), the I/R group (hepatic I/R), and three different VNS treatment groups (hepatic I/R plus VNS). The hepatic I/R group was subjected to portal vein and hepatic artery occlusion for 1 hour followed by 6 hours of reperfusion. The intact afferent and efferent cervical vagal nerves were stimulated throughout the I/R process. During VNS, cervical neural activity was recorded. At the end of the experiment, liver function, the wet to dry (W/D) lung weight ratio, histology of the liver and lung, and inflammatory/oxidative indices were evaluated. We found that VNS significantly mitigated lung injury, as demonstrated by alleviation of pulmonary edema and pathological alterations, by limiting inflammatory cytokine infiltration and increasing antioxidant capability. This proof-of-concept study suggested that VNS may protect patients against lung injury induced by hepatic I/R related to various circumstances. This article is protected by copyright. All rights reserved.