Role of nitric oxide and peroxynitrite anion in lung injury induced by intestinal ischemia-reperfusion in rats
- PMID: 12800248
- PMCID: PMC4611808
- DOI: 10.3748/wjg.v9.i6.1318
Role of nitric oxide and peroxynitrite anion in lung injury induced by intestinal ischemia-reperfusion in rats
Abstract
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 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.
Conclusion: Intestinal IR increases NO and ONOO(-) production in the lung, which may be involved in intestinal IR-mediated lung injury.
Figures
References
-
- Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury. J Pathol. 2000;190:255–266. - PubMed
-
- Rotstein OD. Pathogenesis of multiple organ dysfunction syndrome: gut origin, protection, and decontamination. Surg Infect (Larchmt) 2000;1:217–223; discussion 223-225. - PubMed
-
- Mitsuoka H, Schmid-Schönbein GW. Mechanisms for blockade of in vivo activator production in the ischemic intestine and multi-organ failure. Shock. 2000;14:522–527. - PubMed
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Research Materials
