Neuroleptics (e.g.: chlorpromazine, haloperidol), and anti-emetics (metoclopramide, domperidone) reduce or suppress the emesis induced by the administration of apomorphine.
The administration or the prior ingestion of opiates or barbiturates can induce additive CNS effects and respiratory depression with apomorphine.
Caution is advised when dogs are receiving other dopamine agonist like cabergoline due to possible additive effects such as exacerbation or inhibition of vomiting.
Excessive doses of apomorphine may result in respiratory and/or cardiac depression, CNS stimulation (excitement, seizures) or depression, protracted vomiting, or rarely in restlessness, excitement or even convulsion.
Maropitant or naloxone may be used to reverse the CNS and respiratory effects of apomorphine.
Dopamine antagonists such as metoclopramide should be considered in case of protracted vomiting.
Apomorphine is an aporphine derivative of the dibenzoquinoline class and a synthetic derivative of morphine with no analgesic, opiate or addictive properties. At low doses, apomorphine induces emesis by stimulation of the dopamine receptors in the chemoreceptor trigger zone (CTZ).
Higher doses of apomorphine, however, may suppress vomiting by stimulating the µ receptors in the vomiting centre in the brain.
Absorption
After subcutaneous administration apomorphine is rapidly absorbed. Peak plasma concentration (Cmax) is of 28.10 ± 7.58 ng/ml and is reached after about 20 minutes.
Distribution
Apomorphine is very lipophilic and equilibrates rapidly between blood and tissue. Apomorphine binds extensively to plasma proteins.
Metabolism
Apomorphine is conjugated in the liver (glucuronidation and methylation) into non-active metabolites.
Excretion
Apomorphine is excreted in urine, mostly as the metabolites with some unchanged (<2%). It is also excreted in breast milk. The half-life of the product is 25.9 ± 4.4 minutes.