Abstract
Purpose
The volatile anaesthetics enflurane and isoflurane inhibit the endothelium dependent-relaxation in somein vitro preparations. To determine their site of action on the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway, experiments were conducted in a bioassay system.
Method
Continuously perfused cultured bovine aortic endothelial cells (BAEC were the source of EDRF/NO while a phenytephrine-precontracted denuded rabbit aortic ring, directly superfused by the BAEC effluent served to detect EDRF/NO. The effect of basal and bradykinin (Bk)-stimulated EDRF/NO release on vascular tension was measured The effect of 4% enflurane or 2% isoflurane on EDRF/NO-induced relaxation was determined.
Results
Enflurane added to the perfusate either upstream or downstream in relation to BAEC attenuated the relaxation induced by Bk at low concentrations. On the other hand, isoflurane, added either upstream or downstream to BAEC, potentiated the relaxation induced by the basal release of EDRF but attenuated the relaxation induced by the Bk stimulated release of EDRF Neither enflurane nor isoflurane attenuated the relaxation induced by sodium nitroprusside (SNP), an NO donor.
Conclusion
Enflurane decreases the stability of EDRF/NO released after Bk stimulation while isoflurane can have opposite effects depending on whether the relaxation results from basal or Bk-stimulated release of endothelial derived relaxing factor(s). Isoflurane increases the stability or action of the basal relaxing factor, decreases the stability of the Bk-stimulated relaxing factor (which is probably NO).
Résumé
Objectif
Les anesthésiques volatils enflurane et isolurane inhibent la relaxation dépendante de I’endothélium induite dans des préparations vasculariesin vitro. Des expériences ont été conduites dans un système Bioassay pour déterminer leur site d’action sur la cascade de réaction induite par le facteur relaxant dérivé de I’endothélium/monoxyde d’azote (EDRF/NO).
Méthodic
Des cultures de cellules endothéliales aortiques bovines (CEAB) perfusées en continu constituaient la source de I’EDRF/NO; un anneau aortique de lapin dénudé, préalablement contracté par de la phényléphrine, directement superfusé par I’effluent de CEAB servait à détecter I’EDRF/NO. Nous avons mesuré la relaxation induite sort par la libération basale ou par la libération stimulée par la Bk de facteurs endothéliaux en l’absence et en présence de 4% d’enflurane et de 3% d’isoflurane.
Resultats
Lenflurane ajouté dans le système Bioassay en amont ou en aval relativement aux CEAB atténuait la relaxation induite par Bk a basse concentration. d’autre part. I’lsoflurane ajouté en amont ou en aval des CEAB, potentialisait la relaxation basale de I’EDRF mais atténuait la relaxation induite par la libération d’EDRF provoquée par la stimulation de Bk induite par la libération par la stimulation de Bk. Ni I’enflurane ni l’isoflurane n’atténuait la relaxation induite par le nitroprussiate de sodium (SNP) ou un donneur de NO.
Conclusion
L’enflurane diminue la stabilité de I’EDRF/NO libérée après la stimulation par la Bk; l’isoflurane peut avoir un effet oppose selon que la relaxation résulte de la libération basale ou stimulée par la Bk de I’EDRF. L’isoflurane augmente la stabilite ou I’actrvité du facteur relaxant de base et diminue la stabilité du facteur de relaxation stimulé par le Bk (qui est vraisemblablement le NO).
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This work was funded by the Medical Research Council of Canada.
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Blaise, G., Guy, C., To, Q. et al. Do enflurane and isoflurane interfere with the release, action, or stability of endothelium-derived relaxing factors?. Can J Anaesth 44, 550–558 (1997). https://doi.org/10.1007/BF03011946
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DOI: https://doi.org/10.1007/BF03011946