Ischemia-reperfusion of the pancreas induced hyperresponsiveness of the airways in rats.

OBJECTIVES

Ischemia-reperfusion (I/R) of the rat pancreas induced acute pancreatitis with systemic inflammatory response syndrome. Activated inflammatory cells sequestered in the lung and the proteases released from the inflammatory pancreas both could induce lung inflammation and lung injury.

METHODS

Ischemia of the pancreas was induced by clamping the gastroduodenal and the splenic artery for 2 hours followed by reperfusion for 6 hours. We observed airway reactivity to methacholine. The pulmonary function test of Penh was used to reflect the airway responses. mRNA expression of iNOS and tumor necrosis factor-alpha (TNFalpha) in the lung tissue were measured by real time polymerase chain reactions.

RESULTS

This protocol resulted in significant elevations of the blood concentrations of nitric oxide, hydroxyl radical, amylase, TNFalpha, and white cells among the I/R group. The mRNA expressions of iNOS and of TNFalpha in the lung tissues were significantly increased after I/R. Pulmonary function data showed that I/R of the pancreas induced significant increases in the responses to methacholine challenge: Penh was significantly increased in the I/R group compared with the sham group. Lavage white cells were significantly increased in the I/R group.

CONCLUSIONS

I/R of the pancreas induced systemic inflammatory responses and increased white cell sequestration in the lung. Hyperresponsive responses in the airways of the reperfusion group may be due to airways inflammation, which increased white cell sequesteration in the lung and the expressions iNOS and TNFalpha inflammatory mediators in lung tissues.