Alfentanil is a potent, short acting, opioid analgesic chemically related to fentanyl. The onset of action of alfentanil is more rapid than that of an equianalgesic dose of fentanyl and the maximal analgesic and respiratory depressant effect occurs within 1 to 2 minutes. The duration of action of alfentanil is shorter than that of an equianalgesic dose of fentanyl, and is doserelated. For analgesia lasting longer than 60 minutes, an infusion is preferable. The depressant effect of alfentanil on respiratory rate and alveolar ventilation lasts for a shorter time than that of fentanyl. In most cases, the duration of analgesia exceeds that of the respiratory depression. The duration and degree of respiratory depression tend to be dose-related. At higher doses (>120 micrograms/kg), alfentanil can be used as an anaesthetic induction agent. The induction is smooth, pain-free and devoid of cardiovascular and hormonal stress responses to intubation. The safety margin of alfentanil is comparatively better than that of other opioid analgesics. In rats, the ratio of LD50/ED50 for the lowest level of analgesia for alfentanil is 1080 compared with 4.6, 69.5 and 277 for pethidine, morphine and fentanyl, respectively. Depending upon the dose and speed of administration, alfentanil can cause muscle rigidity, as well as euphoria, miosis and bradycardia, which is common with other opioid analgesics. At doses up to 200 micrograms/kg, alfentanil failed to produce a significant increase in histamine levels or any clinical evidence of histamine release. Recovery after alfentanil administration is rapid and smooth, with a low incidence of post-operative nausea and vomiting.
Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP is located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.
Opioid analgesics bind with stereospecific receptors at many sites within the central nervous system (CNS) to alter processes affecting both the perception of, and emotional response to, pain. Although the precise sites and mechanisms of action have not been fully determined, alterations in the release of various neurotransmitters from afferent nerves sensitive to painful stimuli may be partially responsible for the analgesic effects. It has been proposed that there are multiple subtypes of opioid receptors, each mediating various therapeutic and/or side effects of opioid drugs. The actions of an opioid analgesic may therefore depend upon whether it acts as a full agonist or partial agonist or is inactive at each type of receptor. Fentanyl and its derivatives, including Alfentanil, probably produce their effects via agonist actions at the mu receptor.
Alfentanil has appreciable selectivity for mu receptors in the central nervous system and produces less respiratory depression than morphine or fentalyl at equally analgesic doses. It is one-tenth as potent a respiratory depressant as fentanyl, and one-fourth as potent as fentalyl for analgesia. An anesthestic induction dose of 7 μg/kg produces 5 to 16 minutes of anesthesia and recovery in 2 to 35 minutes.
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