Endogenous Nitric Oxide Protects against Platelet-Activating Factor-Induced Bowel Injury in the Rat

摘要: Platelet-activating factor (PAF) causes bowel necrosis in animal models that is histologically identical to seen neonatal necrotizing enterocolitis, but little known about endogenous mechanisms might protect against PAF-induced injury. We hypothesized nitric oxide represent such a protective mechanism. Adult male Sprague-Dawley rats were pretreated with 2.5 mg/kg NG-nitro-L-arginine methyl ester (L-NAME), potent synthase inhibitor, and given injections of 1.5 micrograms/kg PAF 15 min later. Animals treated normal saline placebo, L-NAME alone, alone also studied. Superior mesenteric artery blood flow pressure continuously recorded. At the end 2 h or upon death animal, hematocrit was measured intestinal samples taken for histologic examination determination myeloperoxidase activity, measure neutrophil content. Compared animals followed by developed significantly worse injury (median scores: versus 0.5, p = 0.005), hemoconcentration (final 65.2 +/- 2.0% 53.9 1.0%, < 0.001), activity (12.45 1.94 U/g 6.51 0.57 U/g, 0.01). The last two effects further accentuated when 10 before PAF. Treatment sodium nitroprusside, donor, after administration reversed L-NAME. phenylephrine rather than did not develop despite comparable reductions superior treatment.(ABSTRACT TRUNCATED AT 250 WORDS)