Inhibition of nitric oxide synthase reduces Sephadex-induced oedema formation in the rat lung: Dependence on intact adrenal function |
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Authors: | S E Andersson L Källström M Malm A Miller-Larsson B Axelsson |
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Institution: | (1) Dept. of Pharmacology, Astra-Draco AB, P.O. Box 34, S-221 00 Lund, Sweden |
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Abstract: | In the present study we have investigated the effect of L-nitro arginine mono methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthase on Sephadex induced inflammation in the rat lung. Instillation of Sephadex into the airways induced an inflammatory reaction characterized by a long-lasting interstitial oedema, measured as an increase in lung weight, and an influx of inflammatory cells into the airways. L-NAME given s.c. prevented the increase in lung weight following Sephadex instillation. The inactive enantiomer D-NAME had no effect, nor did aminoguanidine which indicates that this effect of L-NAME was mediated by inhibition of the constitutive form of NOS. Treatment with L-NAME did not reduce an established oedema. In contrast, L-NAME tended to enhance the influx of oesinophils into the airways of Sephadex-instilled animals.L-NAME did not have any effect on the development of oedema in adrenalectomized rats or in animals where formation of glucocorticosteroids (GCS) was inhibited with metyrapone. L-NAME did not however, increase plasma levels of corticosterone. The present results indicate that, in this model, inhibition of NO-synthesis has marked anti-inflammatory effects. The underlying mechanism is complex but seems not to involve prevention of overproduction of NO. |
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Keywords: | Corticosterone Leucocyte emigration Lung oedema Nitric oxide synthase Sephadex |
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