The neuromuscular effects of lignocaine.
The local anesthetic drug lignocaine, in concentrations which completely block both nerve and muscle action potentials, produces concentration-dependent contractures in the vertebrate skeletal and smooth muscle fibres. The contractures produced by lignocaine were not related to membrane depolarization. Although lignocaine greatly reduced the depolarizations and contractures produced by depolarizing agents, such ACh or carbachol, it had a differential effect on the responses produced by tetraethylammonium (TEA) at the chick neuromuscular junction. Lignocaine reduced the TEA-induced depolarizations while it markedly enhanced the contracture responses. In the absence of membrane depolarization, the contractures produced by lignocaine may be attributed to an effect on release of intracellular calcium (Ca2+) from the sarcoplasmic reticulum (SR). The results suggested a multiple site of action of lignocaine at the vertebrate neuromuscular junction.
D000109:Acetylcholine / Q000037:antagonists & inhibitors; D000818:Animals; D002217:Carbachol / Q000037:antagonists & inhibitors; D008012:Lidocaine / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects; D009467:Neuromuscular Depolarizing Agents / Q000037:antagonists & inhibitors*; D009469:Neuromuscular Junction / Q000187:drug effects*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000037:antagonists & inhibitors
D009467:Neuromuscular Depolarizing Agents; D013757:Tetraethylammonium Compounds; D019789:Tetraethylammonium; D002217:Carbachol; D008012:Lidocaine; D000109:Acetylcholine