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      Nitric oxide inhibits leucocyte migration in carrageenin-induced rat pleurisy.

      Inflammation Research
      Animals, Arginine, administration & dosage, pharmacology, Blood Pressure, Carrageenan, Cell Movement, drug effects, Enzyme Inhibitors, Guanidines, Leukocytes, physiology, Male, Nitric Oxide, Nitric Oxide Donors, Nitric Oxide Synthase, antagonists & inhibitors, Nitric Oxide Synthase Type II, Nitroso Compounds, Pleura, pathology, Pleural Effusion, physiopathology, Pleurisy, chemically induced, Rats, Rats, Wistar

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          Abstract

          The role of nitric oxide (NO) on leucocyte migration has been investigated in rat carrageenin-induced pleurisy. Male Wistar rats. L-arginine, NOC-18 and aminoguanidine were administered subcutaneously 1 h prior to carrageenin injection. Leucocyte accumulation into the pleural cavity was measured 4 h after carrageenin challenge. Statistical significance was calculated by Bonferroni test. L-arginine (10 mg/kg) or the NO donor NOC-18 (10 mg/kg), significantly inhibited leucocyte infiltration by 31% and 20% respectively (P<0.01). On the contrary, when these compounds were given at high doses (L-arginine 300 mg/kg; NOC-18 30 mg/kg), leucocyte accumulation was increased by 22% and 33% respectively (P<0.01). Aminoguanidine, a relatively selective inhibitor of the inducible NO synthase, depending on the dose, showed a biphasic effect on cell migration. Thus, at low doses (30 and 100 mg/kg), aminoguanidine increased (by 40% and 74% respectively, P< 0.01) leucocyte infiltration which was inhibited by 41% (P < 0.01) when the drug was given at high dose (300 mg/kg). These results suggest that in rat carrageenin-induced pleurisy NO primarily inhibits leucocyte migration.

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