Effects of Nicotine and Vagus Nerve in Severe Acute Pancreatitis-Associated Lung Injury in Rats

Objectives 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 alpha 7 nicotinic acetylcholine receptors on immune cells. Experimental evidence indicates that vagus nerve stimulation or alpha 7 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-alpha; 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.