Local anesthetics potentiate nondepolarizing mus-cle relaxant blockade in laboratory experiments, but the clinical importance of this observation is unknown (and probably nil).
Succinylcholine and ester local anesthetics depend on pseudocholinesterase for metabolism. Concurrent administration might conceivably increase the time that both drugs remain unmetabo-lized in the bloodstream. There is likely no actual clinical importance of this potential interaction.
Dibucaine, an amide local anesthetic, inhib-its pseudocholinesterase, and the extent of inhibi-tion by dibucaine defines one family of genetically abnormal pseudocholinesterases . Pseudocholinesterase inhibitors (eg, organophos-phate poisons) can prolong the metabolism of ester local anesthetics (see Table 11–3).
Histamine (H2) receptor blockers and β block-ers (eg, propranolol) decrease hepatic blood flow and lidocaine clearance. Opioids potentiate epidural and spinal analgesia produced by local anesthet-ics. Similarly α2-adrenergic agonists (eg, clonidine) potentiate local anesthetic analgesia produced after epidural or peripheral nerve block injections. Epidural chloroprocaine may interfere with the analgesic actions of neuraxial morphine, notably after cesarean delivery.
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