Published online Jun 15, 2003. doi: 10.3748/wjg.v9.i6.1318
Revised: March 4, 2003
Accepted: March 10, 2003
Published online: June 15, 2003
AIM: To evaluate effects of nitric oxide (NO) and peroxynitrite anion (ONOO-) on lung injury following intestinal ischemia-reperfusion (IR) in rats.
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 min before reperfusion (IR + AG). The lung malondialdehyde (MDA) and nitrate/nitrite (NO2-/NO3-) 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 NO2-/NO3- 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 NO2-/NO3- 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.
CONCLUSION: Intestinal IR increases NO and ONOO- production in the lung, which may be involved in intestinal IR-mediated lung injury.