Abstract
Although thiobarbiturates potentiate, and fentanyl attenuates peripheral vasoconstriction, the intracellular mechanism involved in this phenomenon is not clear. Because smooth muscle contraction induced by α1-adrenoceptor agonists is mediated by the phosphatidylinositol (PI) response, this study was carried out to clarify if thiamylal and fentanyl affect the norepinephrineinduced PI response in rat aortic slices. Rat aortic slices were incubated in Krebs-Henseleit solution containing 5 mM LiCl, [3H]myo-inositol, and varying concentrations of thiamylal or fentanyl. The PI response was stimulated by 0.09 μM (ED50) norepinephrine (NE). The [3H]inositoI monophosphate (IP1) was separated from [3H]myo-inositol by column chromatography and counted with a liquid scintillation counter. The basal IP1, accumulation was not affected by thiamylal and fentanyl. Norepinephrine-induced IP1 accumulation was potentiated by thiamylal at concentrations of 10 μM and 100 μM. Norepinephrine-induced IP1 accumulation was attentuated by 1 μM and 10 μM fentanyl. The results suggest that thiamylal stimulates the NE-induced PI response, which potentiates the vasoconstriction, and fentanyl attentuates NE-induced PI response, which would attenuate the vasoconstriction.
Résumé
On connaît mal le mécanisme intracellulaire qui fait que le thiamylal potentialise la vasoconstriction périphérique et que le fentanyl l’atténue. Comme la constriction du muscle lisse induite par les agonistes α1-adrénergiques dépend de la réponse du phosphatidylinositol (PI), cette étude vise à vérifier sur des tranches d’aorte de rat si le thiamylal et le fentanyl affectent la réponse du PI induite par la norépinéphrine (NE). Cellesci sont incubées dans une solution de Krebs-Henseleit contenant 5 mM de LiCl, du [3H] myo-inositol et différentes concentrations de thiamylal ou de fentanyl. La réponse du PI est provoquée par 0,09 μM (ED50) de NE. Le [3H] inositol monophosphate (IP1) est séparé du [3H] myo-inositol par Chromatographie sur colonne anionique et mesuré avec un compteur à scintillation liquide. L’accumulation d’IP1 initiale n’est pas affectée par le thiamylal et le fentanyl. L’accumulation d’IP1 induite par la NE est potentialisée par le thiamylal à des concentrations de 10 μM et de 100 μM. L’accumulation d’IP1 induite par la NE est atténuée par 1 μM et 10 μM de fentanyl. Ces résultats suggèrent que le thiamylal stimule la réponse induite par la NE, laquelle potentialise la vasoconstriction, et que le fentanyl atténue la réponse de l’IP1 induite par la NE, laquelle pourrait atténuer la vasoconstriction.
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Shibata, O., Todoroki, S., Terao, Y. et al. Phosphatidylinositol responses are involved in the vascular effects of thiamylal and fentanyl. Can J Anaesth 42, 1164–1170 (1995). https://doi.org/10.1007/BF03015106
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DOI: https://doi.org/10.1007/BF03015106