Aim
To evaluate effects of nitric oxide (NO) and peroxynitrite anion (ONOO(-)) on lung injury following intestinal ischemia-reperfusion (IR) in rats.
Conclusion
Intestinal IR increases NO and ONOO(-) production in the lung, which may be involved in intestinal IR-mediated lung injury.
Methods
A rat model of intestinal ischemia was made by clamping superior mesenteric artery and lung injury was resulted from reperfusion. The animals were randomly divided into 3 groups: sham operation (Sham), 2 h ischemia followed by 2 h reperfusion (IR) and IR pretreated with aminoguanidine (AG) - an inhibitor of inducible NO synthase (iNOS) 15 minutes before reperfusion (IR+AG). The lung malondialdehyde (MDA) and nitrate/nitrite (NO(2)(-)/NO(3)(-)) contents and morphological changes were examined. Western blot was used to detect the iNOS protein expression. Immunohistochemical staining was used to determine the change of nitrotyrosine (NT)- a specific "footprint" of ONOO(-).
Results
The morphology revealed evidence for lung edema, hemorrhage and polymorphonuclear sequestration after intestinal IR. Compared with sham group, lung contents of MDA and NO(2)(-)/NO(3)(-) in IR group were significantly increased (12.00+/-2.18 vs 23.44+/-1.25 and 76.39+/-6.08 vs 140.40+/-4.34, P<0.01) and the positive signals of iNOS and NT were also increased in the lung. Compared with IR group, the contents of MDA and NO(2)(-)/NO(3)(-) in IR+AG group were significantly decreased (23.44+/-1.25 vs 14.66+/-1.66 and 140.40+/-4.34 vs 80.00+/-8.56, P<0.01) and NT staining was also decreased.