Drugs to facilitate recovery of neuromuscular blockade and muscle strength.
Several drugs that quicken recovery from neuromuscular blockade caused by vecuronium in anesthetized patients are reviewed. Ulinastatin, a protease inhibitor, is thought to promote the release of acetylcholine at the neuromuscular junction and increases hepatic blood flow and urine volume. For this reason, ulinastatin quickens recovery from neuromuscular blockade in anesthetized patients receiving vecuronium. Additionally, pretreatment with ulinastatin avoids prolongation of vecuronium-induced neuromuscular blockade in patients with hepatic cirrhosis. Gabexate mesilate is also a protease inhibitor. During a continuous infusion of gabexate mesilate, recovery from neuromuscular blockade was quickened. Amino acid-enriched solution supplies energy to the skeletal muscles and causes an increase in muscle strength. An infusion of amino acid-enriched solution hastens recovery from neuromuscular blockade in anesthetized patients. When amino acids supply energy to the skeletal muscles, they simultaneously produce heat in the skeletal muscles. This thermal generation may be closely related to fast recovery from neuromuscular blockade. Amino acid-enriched solution makes recovery from neuromuscular blockade quick and avoids hypothermia during general anesthesia. Milrinone, a phosphodiesterase III inhibitor, is supposed to increase the release of acetylcholine at the neuromuscular junction and make the neuromuscular junction sensitive to acetylcholine. Therefore, recovery from neuromuscular blockade is hastened. Nicorandil enhances membrane K+ conductance in skeletal muscle and increases contraction of the skeletal muscle. Thus, nicorandil quickens recovery from neuromuscular blockade.
Saitoh
Yuhji
Y
Department of Anesthesiology, Satte General Hospital, 4-14-24 Higashi, Satte 340-0114, Japan.
D000596:Amino Acids / Q000494:pharmacology; D000762:Anesthesia Recovery Period; D000818:Animals; D001833:Body Temperature Regulation / Q000187:drug effects; D006801:Humans; D020105:Milrinone / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000294:innervation; D019148:Neuromuscular Blockade; D009469:Neuromuscular Junction / Q000187:drug effects*; D003473:Neuromuscular Nondepolarizing Agents / Q000037:antagonists & inhibitors*; D020108:Nicorandil / Q000494:pharmacology; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D015221:Potassium Channels / Q000819:agonists; D011480:Protease Inhibitors / Q000494:pharmacology; D014673:Vecuronium Bromide / Q000037:antagonists & inhibitors*
D000596:Amino Acids; D003473:Neuromuscular Nondepolarizing Agents; D010726:Phosphodiesterase Inhibitors; D015221:Potassium Channels; D011480:Protease Inhibitors; C117780:mitochondrial K(ATP) channel; D020108:Nicorandil; D014673:Vecuronium Bromide; D020105:Milrinone