Inducible nitric oxide synthase ameliorates lung injury in rat after gut ischemia-reperfusion

2003 Fiscal Year Final Research Report Summary

• Project/Area Number: 13671344
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Digestive surgery
• Research Institution: Tokyo Medical University
• Principal Investigator: YUKIOKA Tetsuo Tokyo Medical University, Medicine, Professor, 医学部, 教授 (00182668)
• Project Period (FY): 2001 – 2003
• Keywords: Gut / ischemia-reperfusion / NO / 一酸化窒素

Research Abstract

BACKGROUND : The nature of the involvement of an inducible nitric oxide (NO) release in acute conditions has been controversial. We sought to determine whether a relatively selective inducible NO synthase inhibitor, aminooguanidine (AG), ameliorates pulmonary microvascular injury after gut ischemia -reperfusion. METHODS : Anesthetized Wistar rats underwent superior mesenteric artery occlusion for 30 mm and reperfusion for 6 hr (I/R) or sham operation (SHAM). Another set of animals undergoing I/R received an aminoguanidine IP (I/R+AG). Pulmonary vascular permeability was assessed by measuring tissue retention of Evans blue, a dye that binds albumin (EBD). RESULTS : The concentrations of NO_2/NO_3 (lung and plasma) in the I/R group were higher than those of the sham (p<0.01). The lung/plasma EBD ratio In the I/R group was also higher than that of the sham. Treatment with the aminoguanidine prevented this lung injury induced by the gut isehemia-reperfusion. CONCLUSION : Increased lung vascular permeability elicited by gut I/R was significantly attenuated with inhibition of an inducible NO release by AG.