Abstract
Purpose
Hypocapnia causes cerebral arterial constriction, whereas volatile anaesthetics cause dilatation. The purpose of this study was to compare the direct effects of halothane, isoflurane and sevoflurane on hypocapniainduced constnction of isolated cerebral arteriesin vitro.
Methods
Basilar and middle cerebral arteries of mongrel dogs (n= 11) were cut into nngs and mounted for isometnc tension recording in organ baths containing Krebs’ bicarbonate solution, aerated with CO2 5% and O2 95% at 37°C. After constnction with 20 mM KCl, hypocapnia was induced by replacing the aerating gas with CO2 2.5% and O2 97.5% in the presence or absence of anaesthetics.
Results
Exposure of cerebroartenal rings to the hypocapnic gas produced sustained vasoconstnction (418 ± 19 mg), reaching a plateau within 10 to 15 min. Halothane (0.5, 1, 2 MAC) attenuated the hypocapnia-induced constnction (P< 0.05). In contrast, isoflurane and sevoflurane attenuated this constriction only at 2 MAC (P< 0.05). Attenuation by halothane was greater than that by isoflurane or sevoflurane at each concentration(P< 0.05). NG-nitro-L-arginine (3 × 10−5 M) did not alter the contractile response to hypocapnia. When a similar degree of constnction was induced by addition of 10 mM KCl, halothane (1 and 2 MAC) preferentially attenuated the constriction induced by hypocapnia to a greater extent than that induced by 10 mM KCl (P< 0.01)
Conclusion
Hypocapnia-induced vasoconstnction of isolated dog cerebral arteries precontracted with KCl is more susceptible to halothane than isoflurane or sevoflurane. This may account for the greater increase in cerebral blood flow dunng halothane than isoflurane or sevoflurane anaesthesia.
Résumé
Objectif
L’hypocapnie provoque une vasoconstriction artérielle cérébrale alors que les anesthésiques volatils provoquent une vasodilatation. Cette étude visait à comparer les effets de l’halothane, de l’isoflurane et du sévoflurane sur la constnction induitein vitro des artères cérébrales par hypocapnie.
Méthodes
Des artères basilaires et cérébrales moyennes de chiens (n= 11) ont été découpées en anneaux et montées dans des bains organiques contenant une solution de Krebs bicarbonatée, aérée avec du CO2 à 5% et de I’O2 à 95% à 37°C. Après constnction avec 20 mM de KCl, l’hypocapnie a été induite en remplaçant le gaz d’aération par du CO2 à 2,5% et de I’O2 à 97,5% avec ou sans anesthésque.
Résultats
Lexposition des anneaux d’artères cérébrales au mélange hypocapnique a produit une vasoconstriction soutenue (418 ± 19 mg) atteignant un plateau en 10 à 15 min. L’halothane (MAC 0.5 et 1.2%) a atténué la vasoconstnction induite par l’hypocapnie (P< 0.05.)Par contre, en présence d’isofiurane et de sevoflurane. cette atténuation n’est survenue qu’à une concentration de 2% (P< 0.05). Avec toutes les concentrations d’halothane. l’atténuation a été plus prononcée que celle produite par l’isoflurane et le sevoflurane (P< 0,05). La Ng-nitro-L-argimne (3 × 10−5 M) n’a pas altéré l’effet contractile de rhypocapnie. Avec un degré de constriction identique induit par l’addition de 10 mM de KCl. l’halothane (MAC 1 et 2) a atténué de façon préférentielle la constriction induite par l’hypocapnie à un degré plus important que la constriction induite par 10 mM de KCl (P< 0,01).
Conclusions
La vasoconstnction induite par hypocapnie d’artères cérébrales canines isolées préalablement contractées avec du KCI est plus susceptible à l’halothane qu’à l’isoflurane et au sévoflurane. Ceci peut expliquer l’augmentation plus importante du débit cérébral pendant ranesthésie à rhalothane que pendant l’anesthésie à l’isoflurane et au sévoflurane.
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Ogawa, K., Yamamoto, M., Mizumoto, K. et al. Volatile anaesthetics attenuate hypocapnia-induced constriction in isolated dog cerebral arteries. Can J Anaesth 44, 426–432 (1997). https://doi.org/10.1007/BF03014465
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DOI: https://doi.org/10.1007/BF03014465