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Dopamine reverses cardiovascular depression of toxic doses of pentobarbitone in dogs

  • Charles Roesch
  • Kenneth A. Haselby
  • Raymond R. Paradise
  • Gopal Krishna
  • Stephen Dierdorf
  • Thomas M. Wolfe
  • Chalapathi C. Rao
Article

Abstract

Pentobarbitone, 20 mg.kg-1 IV followed by infusion of 25 mg.kg-1.hr-1, produced a progressive decrease in mean arterial pressure in dogs from 113 ± 17mmHg (SD) after one hour of infusion to 82 ±21 mmHg after3.5 hours and to 49 ± 22 mmHg after 5.5 hours. EEG silence occurred at 3.6 ± 0.6 hours. In dogs similarly treated with pentobarbitone, a two hour infusion of dopamine 5.µg.kg-1.min-1 beginning at the time of EEG silence prevented the further decrease in pressure and restored pressure to 87 ± 18 mmHg.

The mechanism for this effect of dopamine was an increase in cardiac output as systemic vascular resistance was unaffected by dopamine. The cardiac output increase was mainly the result of an increase in stroke volume as heart rate increased only slightly. Since reduced stroke volume was the main reason why pentobarbitone lowered blood pressure, the effect of dopamine on stroke volume and thus on blood pressure makes it an appropriate antagonist to the cardiovascular effects of toxic doses of pentobarbitone.

Key words

hypnotics: pentobarbitone heart: cardiac output, dopamine brain: electroencephalography 

Résumé

Le pentobarbitone administré à hautes doses (20 mg.kg-1, dose d’attaque suivie d’une infusion de 25 mg.kg-1 par heure) à des chiens a produit une diminution progressive de la pression artérielle moyenne. En effet, chez les animaux ainsi traités la pression artérielle moyenne est passée de 113 ± 17 mmHg après une heure d’infusion à82±21 mmHg après trois heures et demie et à 49 ± 22 mmHg après cinq heures et demie de ce traitement. Le silence encéphalographique s’est établi après 3.6 ± 0.6 hre. Chez d’autres chiens traités de la même façon au pentobarbitone, une infusion de dopamine 5 µg.kg-1par minute pendant deux heures, commencée au début du silence électroencéphalographique, a stoppé la descente de la pression artérielle et l’a rétablie à 87 mmHg ± 18.

C’est par l’augmentation du débit cardiaque que cet effet s’est manifesté car les résistances vasculaires systémiques n’ont pas été modifées par la dopamine. Cette augmentation de débit cardiaque était surtout le résultat d’une augmentation du volume d’éjection car la fréquence cardiaque s’est à peine modifiée. Comme c’est par réduction du volume d’éjection que le pentobarbitone avait diminué la pression artérielle, la dopamine, en rétablissant le volume d’éjection, apparaît donc d’un choix judicieux pour contrer les effets cardiovasculaires indésirables de doses toxiques de pentobarbitone.

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Copyright information

© Canadian Anesthesiologists 1984

Authors and Affiliations

  • Charles Roesch
    • 1
  • Kenneth A. Haselby
    • 1
  • Raymond R. Paradise
    • 1
  • Gopal Krishna
    • 1
  • Stephen Dierdorf
    • 1
  • Thomas M. Wolfe
    • 1
  • Chalapathi C. Rao
    • 1
  1. 1.Departments of Anesthesia and PharmacologyIndiana University Medical CenterIndianapolis

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