| Class | Phosphodiesterase inhibitor |
|---|---|
| Chemistry |
Opioid alkaloid |
| Routes of administration |
IV, but mainly used as an intra-arterial injection |
| Absorption |
Variable, and mainly poor oral absorption; bioavailability is ~50% |
| Solubility |
Completely insoluble in water |
| Distribution |
VOD 20-25L/kg; 95% protein bound |
| Metabolism |
Mainly hepatic metabolism |
| Elimination |
Very rapid distribution half-life (several minutes); overall elimination half life is closer to 100 minutes |
| Time course of action |
Rapid onset and offset of effect; needs to be given as an infusion |
| Target receptor |
Phosphodiesterase 10 (PDE 10) |
| Mechanism of action |
Increases cyclic AMP by inhibiting phosphodiesterase (with maximum selectivity for PDE10), which is responsible for cAMP catabolism. Selective for vascular smooth muscle. |
| Clinical effects |
Vasodilation, tachycardia, hypotension, hepatotoxicity, drowsyness, respiratory depression, hyperthermia, metabolic acidosis, and constipation |
| Literature reference |
Garrett et al, 1978 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |