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Canadian Journal of Anesthesia, Vol 31, 654-658, Copyright © 1984 by Canadian Anesthesiologists' Society

Dopamine Reverses Cardiovascular Depression of Toxic Doses of Pentobarbitone In Dogs

CHARLES ROESCH PHD MD1, KENNETH A. HASELBY MD1, RAYMOND R. PARADISE PHD1, GOPAL KRISHNA MD1, STEPHEN DIERDORF MD1, THOMAS M. WOLFE MD1, and CHALAPATHI C. RAO MD1

1 Departments of Anesthesia and Pharmacology, Indiana University Medical Center, Indianapolis, IN

Address correspondence to: Kenneth Haselby, MD, Department of Anesthesia, Indian University School of Medicine, Indianapolis IN 46223.

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 ± 17 mmHg (SD) after one hour of infusion to 82 ± 21 mmHg after 3.5 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 -1 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






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Copyright © 1984 by the Canadian Anesthesiologists' Society.