Background:
Intraabdominal surgery is commonly accompanied by gastrointestinal motility changes. Although the mechanism is multifactorial, inflammation of the intestinal muscularis is key event. Our aim was to investigate the functional consequences of inhaled methane on intestinal motility changes in a rat model of antigen–independent inflammation.

Material and Methods:
The effects of a 50–min intestinal ischemia followed by 120–min reperfusion were monitored in anesthetized rats. Control, IR and IR+methane inhalation groups (normoxic artificial air with 2.2% methane, in the last 5 min of ischemia and 10 min during reperfusion) were used (n=8 each). Intestinal myoelectrical activity was monitored and the integral of intestine–specific dominant frequency ranges was analysed. At the end of reperfusion, quantitative histochemical (nNOS and eNOS immunohistochemistry) and biochemical (xanthine oxidoreductase (XOR), nitrite/nitrate and nitrotyrosine) analyses were performed.

Result:
After IR the intestinal myoelectrical activity decreased, while the levels of nitrite/nitrate, nitrotyrosine, and XOR were increased significantly. The number of total myenteric neurons did not change but the density of nitrergic myenteric neurons was significantly elevated. Normoxic methane inhalation increased the post–ischemic intestinal motility significantly, neutralized the IR–induced effects on nitrergic neuronal density changes, and reduced the XOR activity and the signs of reactive nitrogen species generation.

Conclusion:
Normoxic methane inhalation prevents motility dysfunction through resetting of nitrergic myenteric function and inhibition of IR–induced oxido–nitrosative stress.
Supported by OTKA K104656, TAMOP 4.2.2A–11/KONV–2012–0035 and co–financed by the European Social Fund in the framework of TÁMOP–4.2.4.A/2–11/1–2012–0001 ‘National Excellence Program’.