Sufentanil Powder is an Opioid Agonist. The mechanism of action of sufentanil is as a Full Opioid Agonist. Sufentanil PowderSufentanil is an opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent. It is administered by the intravenous, epidural and Sufentanil Powder routes. Also known as Dsuvia, the sublingual form is used for the management of acute pain in adults that is severe to warrant the use of an opioid analgesic in certified medically supervised healthcare settings, including hospitals, surgical centers, and emergency departments. Consideration may be made in the future for the use of the sublingual form in the US military in cases where analgesia is required immediately.
Drug and Medication Information
Drug Indication of Sufentanil Powder
The indications for this drug are as follows:
- 1. As an analgesic adjunct in the maintenance of balanced general anesthesia in patients who are intubated and ventilated.
- 2. As a primary anesthetic agent for the induction and maintenance of anesthesia with 100% oxygen in patients undergoing major surgical procedures, in patients who are intubated and ventilated, such as cardiovascular surgery or neurosurgical procedures in the sitting position, to provide favorable myocardial and cerebral oxygen balance or when extended postoperative ventilation is anticipated.
- 3. For epidural administration as an analgesic combined with low dose (usually 12.5 mg per administration) bupivacaine usually during labor and vaginal delivery.
- 4. The sublingual form is indicated for the management of acute pain in adults that is severe to warrant the use of an opioid analgesic in certified medically supervised healthcare settings, including hospitals, surgical centers, and emergency departments.
Mechanism of Action
Sufentanil Powder is a synthetic, potent opioid with highly selective binding to ?-opioid receptors [F2009]. These receptors are widely distributed in the human brain, spinal cord, and other tissues [A39636], [A39637]. In general, opioids decrease cAMP (affecting neural signaling pathways), decrease neurotransmitter release, and cause membrane hyperpolarization, all of which contribute to the relief of painful symptoms [A39637]. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic neural transmission via G-proteins that activate effector proteins. Binding of the opiate receptor leads to the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP, located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. The release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is then inhibited [A39637]. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist), also preventing neurotransmitter release [A39637]. Sufentanil and other opioids open calcium-dependent inwardly rectifying potassium channels, resulting in hyperpolarization and reduced neuronal excitability [A39636], [A39637].