title: Effects of Nicotine and Vagus Nerve in Severe Acute Pancreatitis-Associated Lung Injury in Rats.
abstract: OBJECTIVE
  The cholinergic anti-inflammatory pathway has been elucidated as a regulator of inflammatory responses in several experimental models of diseases. This regulatory mechanism is mediated by acetylcholine, released from efferent vagus nerve, interacts with α7 nicotinic acetylcholine receptors on immune cells. Experimental evidence indicates that vagus nerve stimulation or α7 nicotinic acetylcholine receptor agonists control proinflammatory cytokine production and protect animals in diverse lethal models. The aim of the study was to investigate effect of the cholinergic anti-inflammatory pathway in acute lung injury in an experimental model of severe acute pancreatitis (SAP).
  
  
  METHODS
  In taurocholate-induced SAP in rats, pancreatitis was preceded by pretreatment with the nicotinic receptor agonist nicotine or unilateral left cervical vagotomy.
  
  
  RESULTS
  Pretreatment with nicotine strongly alleviated severity of SAP-associated lung injury through attenuating serum amylase, lipase, and interleukin 6 levels; pancreas and lung pathological injury; lung myeloperoxidase activity; lung tumor necrosis factor-α; and high-mobility group box 1 expression. Inversely, vagotomy pretreatment resulted in an enhanced severity of pancreatitis and lung injury.
  
  
  CONCLUSIONS
  Our results reveal the role of the cholinergic anti-inflammatory pathway in experimental SAP-associated lung injury; nicotine pretreatment exerts a protective effect and vagotomy pretreatment exerts the opposite effect.
authors.affiliation: From the *Department of Hepatobiliary and Laparoscopic Surgery, Renmin Hospital of Wuhan University, Wuhan; and †Department of General Surgery, Affiliated Hospital of Hubei University of Medicine, Xiangyang, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Ma
authors.forename: Kaihuan
authors.initials: K
authors.lastname: Yu
authors.forename: Jia
authors.initials: J
authors.lastname: Yu
authors.forename: Weixing
authors.initials: W
authors.lastname: Wang
authors.forename: Youming
authors.initials: Y
authors.lastname: Ding
authors.forename: Chen
authors.initials: C
authors.lastname: Chen
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Chen
authors.forename: Kailiang
authors.initials: K
authors.lastname: Zhao
authors.forename: Teng
authors.initials: T
authors.lastname: Zuo
authors.forename: Xiaobo
authors.initials: X
authors.lastname: He
authors.forename: Qiao
authors.initials: Q
authors.lastname: Shi
authors.forename: Jun
authors.initials: J
authors.lastname: Ren
mesh_terms: D000208:Acute Disease; D055371:Acute Lung Injury / Q000503:physiopathology / Q000517:prevention & control*; D000681:Amylases / Q000097:blood; D000818:Animals; D015153:Blotting, Western; D005260:Female; D024243:HMGB1 Protein / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood; D008049:Lipase / Q000097:blood; D008168:Lung / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology; D010195:Pancreatitis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D009195:Peroxidase / Q000378:metabolism; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013656:Taurocholic Acid; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014628:Vagotomy; D014630:Vagus Nerve / Q000503:physiopathology* / Q000601:surgery
chemical_list: D024243:HMGB1 Protein; D015850:Interleukin-6; D018722:Nicotinic Agonists; D014409:Tumor Necrosis Factor-alpha; D013656:Taurocholic Acid; D009538:Nicotine; D009195:Peroxidase; D008049:Lipase; D000681:Amylases