Abstract
Purpose
Halothane suppresses platelet aggregationin vitro and ex vivo, and prolongs bleeding time. In a previous invitro study we demonstrated that sevoflurane had a more suppressive effect on platelet aggregation than did halothane. The present study investigated whether the clinical use of sevoflurane affected platelet aggregationex vivo.
Methods
Thirty-eight patients undergoing minor elective surgery were divided randomly into sevoflurane and isoflurane groups. Anaesthesia was induced with thiopentoneiv, and was maintained with sevoflurane or isoflurane with nitrous oxide. Blood was collected to measure platelet aggregation induced by adenosine diphosphate (ADP) and epinephrine. The first (control) blood collection was performed in the operating room before induction of anaesthesia, and the second 5–10 min after tracheal intubation but before the start of surgery, when the end-expiratory sevoflurane or isoflurane concentrations had stabilised at 1–1.5 times the minimum alveolar concentration (MAC) and mean artenal pressures were between 80–120% of preanaesthetic values.
Results
In all samples obtained dunng sevoflurane anaesthesia (n= 15), ADP and epinephnne could not induce secondary aggregation, although they did induce pnmary aggregation. In contrast, in the isoflurane group, both primary and secondary aggregation were observed in 14 out of 15 patients, and secondary aggregation was abolished in only one of the samples obtained dunng anaesthesia.
Conclusion
Sevoflurane, but not isoflurane, alters platelet aggregation in the clinical situation, possibly by suppression of thromboxane A2 formation.
Résumé
Objectif
L’halothane inhibe l’agrégation plaquettairein vitro etin vivo et prolonge le temps de saignement. Nous avons anténeurement démontré que le sévoflurane avait un effet inhibiteurin vitro plus important sur l’agrégation plaquettaire que l’halothane. La présente étude a pour but de vérifier si l’usage clinique du sévoflurane affecte l’agrégation plaquettairein vivo.
Méthodes
Trente-huit patients soumis à une chirurgie élective mineure répartis au hasard en groupe sévoflurane et groupe isoflurane participaient à l’étude. L’anesthésie était induite au thiopentaliv, et entretenue au sévoflurane ou à l’isoflurane avec du protoxyde d’azote. Du sang était recueilli pour la mesure de l’agrégation plaquettaire induite par le diphosphate d’adénosine (ADP) et l’épinéphnne. Le premier échantillon sanguin (contrôle) était recueilli en salle d’opération avant l’induction de l’anesthésie et le second, 5–10 min après l’intubation trachéale et avant le début de l’intervention après stabilisation des concentrations télé-expiratoires de sévoflurane et d’isoflurane à 1–1,5 fois la concentration alvéolaire minimale (MAC) de même que de la pression arténelle moyenne à 80–120% des valeurs préanesthésiques.
Résultats
Malgré une agrégation primaire, l’ADP et l’épinéphnne n’ont induit l’agrégation secondaire dans aucun des échantillons recueillis sous anesthésie au sévoflurane (n = 15). Par contre, on a observé dans le groupe isoflurane une aggrégation tant primaire que secondaire chez 14 des 15 patients, l’agrégation secondaire n’ayant été abolie que chez un seul des patients.
Conclusion
En clinique, le sévoflurane contrairement à l’isoflurane altère l’agrégation plaquettaire possiblement par suppression de la formation de thromboxane A2.
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Hirakata, H., Nakamura, K., Sai, S. et al. Platelet aggregation is impaired during anaesthesia with sevoflurane but not with isoflurane. Can J Anesth 44, 1157–1161 (1997). https://doi.org/10.1007/BF03013337
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DOI: https://doi.org/10.1007/BF03013337