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Inhibition of nitric oxide synthase reduces Sephadex-induced oedema formation in the rat lung: dependence on intact adrenal function

Andersson, Sven LU ; Kallstrom, L; Malm, M; Miller-Larsson, A and Axelsson, B (1995) In Inflammation Research 44(10). p.418-422
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,... (More)
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. (Less)
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author
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Corticosterone, Leucocyte emigration, Lung oedema, Nitric oxide synthase, Sephadex
in
Inflammation Research
volume
44
issue
10
pages
418 - 422
publisher
Birkhaüser
external identifiers
  • pmid:8564517
  • scopus:0028882251
ISSN
1420-908X
DOI
10.1007/BF01757698
language
English
LU publication?
no
id
8afa64f2-be27-4107-a76c-c7f3666f20d4 (old id 1109795)
date added to LUP
2008-07-29 15:48:51
date last changed
2017-01-01 04:49:30
@article{8afa64f2-be27-4107-a76c-c7f3666f20d4,
  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.},
  author       = {Andersson, Sven and Kallstrom, L and Malm, M and Miller-Larsson, A and Axelsson, B},
  issn         = {1420-908X},
  keyword      = {Corticosterone,Leucocyte emigration,Lung oedema,Nitric oxide synthase,Sephadex},
  language     = {eng},
  number       = {10},
  pages        = {418--422},
  publisher    = {Birkhaüser},
  series       = {Inflammation Research},
  title        = {Inhibition of nitric oxide synthase reduces Sephadex-induced oedema formation in the rat lung: dependence on intact adrenal function},
  url          = {http://dx.doi.org/10.1007/BF01757698},
  volume       = {44},
  year         = {1995},
}