Trial reportInflammopharmacology2010
L-arginine reverses cigarette-induced reduction of fractional exhaled nitric oxide in asthmatic smokers.
Trial report in Inflammopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 6 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionComplex mechanisms regulate nitric oxide (NO) synthesis. Cigarette smoking decreases fractional exhaled NO (FE(NO)), while asthmatic inflammation increases FE(NO). To assess whether the smoking-induced decrease in FE(NO) levels was reversible, asthmatic and non-asthmatic smokers inhaled the NO synthase (NOS) substrate, L-arginine. Aminoguanidine, a relatively selective Type II NOS inhibitor, was used also to assess the role of NOS subtypes in these changes of FE(NO).
methodsThe study was a single-blinded, placebo-controlled, cross-over design in two parts. Part I: smoking asthmatic and non-asthmatic smoking subjects smoked one cigarette and then inhaled nebulised L-arginine or L-alanine (control). Spirometry, FE(NO), nasal NO (FN(NO)), FE(CO), were measured for 4 h. Part II: subjects inhaled nebulised aminoguanidine prior to an identical protocol as in Part I. Change in FE(NO) was assessed as area under the curve (AUC).
resultsPart I: In asthmatic smokers, cigarette smoking followed by L-arginine caused a significant median increase in AUC of 29.2(17)% FE(NO) change/hour (p = 0.04), which did not occur in non-asthmatic smokers (baseline FE(NO) 12.7(7.1-18) vs. 6.7(4-9.2) ppb, respectively). Part II: Aminoguanidine prior to smoking caused a significant fall in FE(NO) in both asthmatic and non-asthmatic smokers. L-arginine showed significant reversal of this effect in both asthmatic and non-asthmatic subjects.
conclusionsIn asthmatic smokers, L-arginine increases FE(NO) after cigarette smoking but not in non-asthmatic smokers. The decrease in FE(NO) after aminoguanidine and subsequent partial reversal by L-arginine in both groups, suggests that Type II NOS contributes to the FE(NO) in both.
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