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  • Title: Nitrosoglutathione improves blood perfusion and flap survival by suppressing iNOS but protecting eNOS expression in the flap vessels after ischemia/reperfusion injury.
    Author: Kuo YR, Wang FS, Jeng SF, Lutz BS, Huang HC, Yang KD.
    Journal: Surgery; 2004 Apr; 135(4):437-46. PubMed ID: 15041968.
    Abstract:
    BACKGROUND: The effects of nitric oxide (NO) on the microcirculation and free tissue survival remain controversial. With the use of a rat inferior epigastric artery flap as an ischemia/reperfusion injury (I/R) model, we investigated whether exogenous NO donation regulates endogenous NO synthase (NOS) expression in the flap vessels and promotes flap survival. METHODS: Thirty minutes before flap reperfusion, normal saline (1 ml), nitrosoglutathione (GSNO 0.2, 0.6, 3 mg/kg), or N(G)-nitro-L-arginine-methyl ester (L-NAME, 450 mg/kg), was injected intravenously into 20 rats. Total plasma NOx (NO(2)-/NO(3)-) was measured to reflect NO production. Immunohistochemical staining was investigated for the endothelin-1 (ET-1) and NOS isoforms expression on the flap vessels. NOS isoforms expression was evaluated by Western blot. Laser-Doppler flowmetry monitored flap perfusion. Survival areas were assessed by gross examination at 7 days postoperatively. RESULTS: Flap ischemia at 12 hours followed by reperfusion resulted in endothelial cell damage, as demonstrated by induction of iNOS and ET-1 expression in the flap vessels. An optimal dose of nitrosoglutathione (0.6 mg GSNO/kg) significantly increased plasma NOx levels (P=.027) and improved flap perfusion by laser Doppler measurement (P=.014), and increased the flap viability area (P<.001). Additionally, it selectively suppressed iNOS induction, but enhanced eNOS expression and decreased ET-1 deposition in the flap vessels. In contrast, an NOS inhibitor, N(G)-nitro-L-arginine methyl ester, inhibited both iNOS and eNOS expression in the flap vessels, decreased endogenous NOx production, and compromised flap viability. CONCLUSION: This study indicates that intravenous administration of exogenous GSNO can appropriately donate NO to suppress iNOS induction and enhance eNOS expression in pedicle vessels, resulting in better blood perfusion and a higher flap survival after I/R injury.
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