Dopamine reverses cardiovascular depression of toxic doses of pentobarbitone in dogs.
Pentobarbitone, 20 mg X kg-1 IV followed by infusion of 25 mg X kg-1 X 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 micrograms X kg-1 X 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.
D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D004298:Dopamine / Q000494:pharmacology*; D004569:Electroencephalography; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D008297:Male; D010424:Pentobarbital / Q000037:antagonists & inhibitors / Q000633:toxicity*; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D010424:Pentobarbital; D004298:Dopamine