Abstract

The nervous system interacts dynamically with the immune system to modulate inflammation through humoral and neural pathways. However, the influence of visceral nerve (VN) on acute necrotizing pancreatitis (ANP) has drawn little attention. To investigate the influence of VN on the pathophysiological process of ANP in dogs. The dogs were divided into a sham operation (SO) group, ANP group, ANP + vagal nerve trunk transection (VNTT) group, and ANP + greater splanchnic nerve transection (GSNT) group. The VNTT and GSNT groups underwent VNTT and GSNT respectively immediately after ANP induction. The levels of serum pancreatic amylase (AMY), calcium, high-sensitivity C-reactive protein (HCRP), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were monitored dynamically and the pathological examinations of the pancreas was performed at postoperative day 7. All serum parameters among the four groups showed no differences before the experiment (p > 0.05). At different postoperative times, the serum TNF-α, IL-1β, HCRP, and AMY were significantly increased, however, the serum calcium and IL-10 had dropped in the ANP group versus SO group (p < 0.05); an alike variation trend occurred between the VNTT group and ANP group (p < 0.05); an opposite variation trend occurred between the GSNT group and the ANP group (p < 0.05). The pancreas pathological scoring of VNTT group was highest in the four groups (p < 0.05) and GSNT group was lower versus ANP group (p < 0.05). The GSNT has been shown to alleviate development of ANP, however, VNTT may exacerbate the ANP.

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