ArticleBritish journal of pharmacology1993
A comparison of the effects of polyarginine and stimulated eosinophils on the responsiveness of the bovine isovolumic bronchial segment preparation.
Article in British journal of pharmacology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Distribution of major basic protein on human airway following in vitro eosinophil incubation.Mediators of inflammation · 2010Article
- Deficiency of nitric oxide in polycation-induced airway hyperreactivity.British journal of pharmacology · 1999Article
- Augmentation by eosinophils of gelatinase activity in the airway mucosa: comparative effects as a putative mediator of epithelial injury.British journal of pharmacology · 1996Article
- Stimulated eosinophils and proteinases augment the transepithelial flux of albumin in bovine bronchial mucosa.British journal of pharmacology · 1993Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The bovine isovolumic bronchial segment preparation has been used to study the sensitivity and responsiveness of bronchial smooth muscle after various manipulations. 2. Addition of acetylcholine (ACh) to the lumen of the segments elicited an increase in intraluminal pressure as a result of contraction of the airway smooth muscle. However, the increases in intraluminal pressure were greater when the ACh was added to the adventitial surface of the preparation. 3. Addition of polyarginine to the bronchial lumen for 60-120 min resulted in an increased magnitude of response and greater than 100 fold increase in sensitivity to ACh administered into the lumen. Depolarizations induced by KCl were similarly enhanced when the solution was added into the lumen. In contrast, the sensitivity and responsiveness to ACh or K(+)-induced depolarization administered adventitially was unchanged. 4. The mechanical disruption of the epithelium produced a 32 fold increase in sensitivity to ACh introduced via the lumen, whereas the sensitivity to ACh added adventitially remained unaltered. 5. Addition of polyarginine to the adventitial bathing medium resulted in no change in the responsiveness or sensitivity to ACh, irrespective of whether the ACh was given intraluminally or adventitially. 6. Histological examination revealed that polyarginine caused extensive disordering of the normal architecture of the bronchial epithelium. Taken together with the unaltered responsiveness to adventitial ACh (i.e. lack of change in intrinsic muscle sensitivity) these observations suggest that the effect of polyarginine was most likely due to disruption of a diffusion barrier. 7. In contrast to the effects of polyarginine, the only effect of stimulated eosinophils was to produce a small diminution in the responsiveness to ACh that had been added adventitially.
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Registered trials
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