ArticleJournal of anesthesia1996
Effects of phenol on vascular smooth muscle in rabbit mesenteric resistance arteries.
Article in Journal of anesthesia, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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3 authors at 1 institution in 1 country.
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Abstract
Although phenol has long been used clinically as a neurolytic agent or as a preservative for injections, little information is available regarding its direct vascular action. We therefore studied the effects of phenol (0.1 μM-2mM) on isolated rabbit small mesenteric arteries, using isometric tension recording methods. All experiments were performed on endothelium-denuded strips. Phenol (≥10 μM) generated transsient contractions in a concentration-dependent manner in both normal Krebs and Ca(2+)-free solutions with EC50 values (concentrations that produced 50% of the maximal response) of 39.8 μM and 99.7 μM, respectively. Depletion of intracellular Ca(2+) stores by A23187 or ryanodine completely elimited the phenol-induced contractions. When caffeine (10 mM) and noradrenaline (NA, 10μM) were consecutively applied in Ca(2+)-free solution with an interval of 7 min (sufficient to prevent caffeine-induced inhibition of Ca(2+) sensitivity), caffeine eliminated the contractions induced by subsequent application of NA. In similar experiments where phenol (1 mM) and NA (10 μM) were consecutively applied in Ca(2+)-free solution, phenol significantly inhibited contractions induced by subsequent application of NA. Phenol (0.1 mM, ∼EC65), applied in the presence of either 128 mM K(+) or NA (10 μM), produced transient vasoconstrictions superimposed on both high K(+)-and NA-induced contractions, but had a lesser effect on maintenance of these contractions. The vascular responses to high K(+), NA, and caffeine after washout of phenol were not significantly different from those before application of phenol (up to 2 mM). The results suggest that phenol stimulates Ca(2+) release from intracellular Ca(2+) stores, which are sensitive to both caffine and NA in this resistance artery. The effect does not appear to reflect a toxic effect on vascular smooth muscle. It seems unlikely that phenol causes adverse hemodynamic changes because of the observed direct vascular action.
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