Cardiovascular effects of N-allyl clonidine (ST 567, alinidine): a substance with specific bradycardiac action during neuroleptanesthesia in humans.
The cardiocirculatory effects of N-allyl clonidine (ST 567, alinidine), a substance with specific bradycardiac action at the sinus node [Kobinger et al. 1979], were studied in 30 patients undergoing noncardiac surgery in neuroleptanesthesia. Alinidine (0.5 mg/kg i.v.) alleviated both spontaneous and reactive tachycardia, i.e., in response to deliberate hypotension with sodium nitroprusside (3.0 +/- 1.8 micrograms/kg i.v.), (decrease in heart rate from control: 20.7 +/- 5.7% and 25.4 +/- 3.2%, respectively), without affecting mean arterial blood pressure substantially. The slight but significant reduction in cardiac output can be explained, at least in part, by the decrease in heart rate, since the left ventricular stroke volume showed a tendency to increase and the mean pulmonary artery pressure failed to change significantly. Thus, alinidine may be useful for reducing heart rate and myocardial oxygen consumption in patients under neuroleptanesthesia.
D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000187:drug effects; D002317:Cardiovascular Agents / Q000494:pharmacology*; D003000:Clonidine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008875:Middle Aged; D009458:Neuroleptanalgesia; D009599:Nitroprusside / Q000494:pharmacology
D002317:Cardiovascular Agents; D009599:Nitroprusside; C022192:alinidine; D003000:Clonidine