ArticleMediators of inflammation1996
Rat intestinal mast cell amines are released during nitric oxide synthase inhibition in vitro.
Article in Mediators of inflammation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Inhibition of NO-synthase and degranulation of rat omental mast cells in vitro.Mediators of inflammation · 1996Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of nitric oxide synthase increases microvascular permeability in rat small intestinal villi. To determine the mechanism(s) whereby this occurs we have perfused the vasculature of rat isolated small intestines with a gelatin-containing physiological salt solution. Inclusion of N-nitro-L-argintne methyl ester (L-NAME, 100 muM) or indomethacin (1 muM) in the perfusate increased leakage of injected colloidal carbon into microvessel walls. Pre-treatment with sodium nitroprusside (10 muM) significantly reduced the effects of both L-NAME and indomethacin, whereas carbacyclin (1 muM) only reduced the effects of indomethacin. PD151242 (1 muM) showed some antagonism towards the effects of L-NAME, but nordihydroguaiaretic acid (3 muM) was inactive. Pre-tment with cyproheptadine (10 muM) reduced the effects of both L-NAME and indomethacin, and also significantly reduced background (control) colloidal carbon leakage. Small intestines from polymixin B-treated rats showed significantly reduced colloidal carbon leakage in response to L-NAME. This suggests that the leakage-enhancing effects of both L-NAME and indomethacin in this preparation may be mediated by mast cell-derived amines.
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