ArticleAgents and actions1993
Involvement of protein kinase C in the control of microvascular permeability to colloidal carbon.
Article in Agents and actions, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Rate of perfusion modulates colloidal carbon leakage from rat intestinal microvessels in vitro.Mediators of inflammation · 1995Article
- Vasoconstriction in rat isolated mesentery and small intestine in response to various activators of protein kinase C.Agents and actions · 1994Article
- Stimulation of protein kinase C activity may increase microvascular permeability to colloidal carbon via alpha-isoenzyme.Inflammation · 1994Article
- Lectin-induced increase in microvascular permeability to colloidal carbon in vitro may involve protein kinase C activation.Agents and actions · 1994Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vasculature of the rat small intestine and attached mesentery was perfused in vitro with a gelatin-containing physiological salt solution (GPSS). The inclusion of colloidal carbon (CC) in the perfusate towards the end of the experimental period enabled the "leakiness" of microvessels in the villi to be determined, since "leaky" vessels trap CC in their walls. Addition to the perfusate of the inflammatory agonists platelet-activating factor (PAF, 5 x 10(-6) M) or 5-hydroxytryptamine (5-HT, 1 x 10(-4) M), or the microtubule-disrupting agents podophyllotoxin (5 x 10(-5) M), or colcemid (5 x 10(-5) M), or the protein kinase C (PKC) activator phorbol 12, 13-dibutyrate (PDB, 1 x 10(-6) M), caused significantly increased microvascular "blackening" as assessed by image analysis. 4 alpha-phorbol 12, 13-didecanoate (PDD, 1 x 10(-6) M) had no effect. Pretreatment with the PKC inhibitor Ro 31-8220 [corrected] (1 x 10(-6) M) significantly reduced the effects of PAF, 5-HT and PDB, but not those of podophyllotoxin or colcemid. These results suggest, therefore, that PKC is involved in the permeability-enhancing effects of PAF, 5-HT and PDB. Pretreatment with indomethacin (1 x 10(-6) M) as a cyclooxygenase inhibitor did not reduce the response to PDB, indicating that prostaglandin release is of minor importance in the PDB-induced increase in microvascular permeability.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.