Abstract
Purpose
Propofol may cause hypotension and the mechanism is complex. The present study was designed to determine the direct actions of propofol in medulla of cats.
Methods
Mean systemic arterial pressure (MSAP), heart rate (HR) and cardiac contractility (dp/dt) were compared before and after administration of propofol through the femoral vein (2, 3 or 4 mg · kg−1), vertebral artery (1 mg · kg−1) or the lateral cerebral ventnricle (0.5 mg · kg−1) in eight anaesthetized cats. To study the direct effect of propofol in medulla, pressor areas of the dorsomedial medulla (DM) and rostral ventrolateral medulla (RVLM), or the depressor area of the caudal ventrolateral medulla (CVLM) were first identified with electrical stimuli and then confirmed by pressure microinjection of glutamate (Glu, 0.25M, 30 nl) via a multibarrel-micropipette in 28 cats. One hour later, propofol (0.001%, 50 nl) was microinjected at the same site. Electrical stimulation and Glu were applied again to compare changes of SAR HR and dp/dt with that of the control.
Results
Propofol dose-dependently decreased SAR HR and cardiac contractility. The percent increase of MSAP induced by Glu were reduced by propofol in DM (59 ± 3 % vs 13 ± 2 %, n = 11.P < 0.01) or in RVLM (56 ± 4 % vs 18 ± 2 %, n = 9,P < 0.01). In CVLM, propofol slightly but not significantly increased the depressor responses elicited by Glu (−27 ± 2 %vs ∼-33 ± 3 %. n = 5,P > 0.05).
Conclusion
Our results show that propofol principally inhibits the vasomotor mechanism in the dorsomedial and ventrolateral medulla to effect its hypotensive actions.
Résumé
Objectif
Le propofol produit de l’hypotension par un mécanisme complexe. Cette étude avait pour objectif de délimiter sur le bulbe du chat l’activité directe du propofol.
Méthodes
La pression artérielle systémique moyenne (PASM), la fréquence cardiaque (FC) et la contractilité cardiaque (dp/dt) ont été comparées avant et après l’injection de propofol dans la veine fémorale (2, 3 et 4 mg · kg−1), l’artère vertébrale (1 mg · kg−1) et le ventricule cérébral latéral (0, 5 mg · kg−1) chez six chats anesthésiés. Pour étudier les effets bulbaires directs du propofol, les zones vasopressives dorsomédiane (DM) et ventrolatérale rostrale (BVLR) bulbaires, ou la zone vasodépressive ventrolatérale caudale (BVLC) bulbaire ont d’abord été identifiées par stimulation électrique et confirmées par micro-injection sous pression de glutamate (Glu 0.25M, 30 ml) à l’aide d’une micropipette à plusieurs banllets chez 28 chats. Une heure plus tard, du propofol (0, 001%, 50 nl) était injecté au même site. Lélectrostimulation et Glu étaient appliqués encore une fois pour comparer les changements de PAS. le FC et de dp/dt avec ceux du contrôle.
Résultats
Dépendaminent de la dose, le propofol diminue PAS, FC etdp/dt. En pourcentage, l’augmentation de PASM induite par Glu était réduite par le propofol dans DM 159 ± 3 %va 13 ± 2 %. n= 11,P < 0, 01) ou dans BLVR (56 ± 4 %vs 18± 2%, n = 9, P < 0.01). Dans BLVM, le propofol a augmenté légèrement mais non significativement les réponses vasodépressives induites par Glu (−27 ± 2 % vs −33 ± 3 %. n = 5,P < 0, 05).
Conclusion
Nos résultats montrent que l’action hypotensive du propofol est causée par l’inhibition du mécanisme vasomoteur au niveau des zones bulbaires dorsomédiane et ventrolatérale.
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Yang, CY., Luk, HN., Chen, SY. et al. Propofol inhibits medullary pressor mechanisms in cats. Can J Anaesth 44, 775–781 (1997). https://doi.org/10.1007/BF03013394
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DOI: https://doi.org/10.1007/BF03013394