Inhibition of nitric oxide synthase reduces Sephadex-induced oedema formation in the rat lung: dependence on intact adrenal function
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1109795
- author
- Andersson, Sven LU ; Kallstrom, L ; Malm, M ; Miller-Larsson, A and Axelsson, B
- publishing date
- 1995
- 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
- Birkhäuser Verlag
- 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
- 2016-04-01 12:05:18
- date last changed
- 2021-01-03 05:32:18
@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}}, keywords = {{Corticosterone; Leucocyte emigration; Lung oedema; Nitric oxide synthase; Sephadex}}, language = {{eng}}, number = {{10}}, pages = {{418--422}}, publisher = {{Birkhäuser Verlag}}, 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}}, doi = {{10.1007/BF01757698}}, volume = {{44}}, year = {{1995}}, }