dtubocurarine

d-tubocurarine is a nondepolarizing neuromuscular blocking agent originally derived from curare plants and historically used to induce skeletal muscle relaxation during anesthesia. It is a bis-quaternary ammonium alkaloid that acts at the neuromuscular junction as a competitive antagonist of nicotinic acetylcholine receptors (Nm), thereby preventing acetylcholine from activating motor endplates and causing flaccid paralysis without affecting consciousness or sensation at clinical doses.

Pharmacology and administration are characterized by intravenous delivery with onset typically in 3 to 5 minutes and a duration of about 60 to 90 minutes, though effects can be longer in some patients. It does not readily cross the blood–brain barrier, so it has no direct central nervous system effects. Metabolism is limited, and the drug is cleared mainly by hepatic pathways with renal excretion of metabolites. Because d-tubocurarine can cause histamine release, it may contribute to hypotension and bronchospasm, and it can also produce ganglionic blockade that affects blood pressure and heart rate. Its use can be complicated in patients with myasthenia gravis or significant hepatic or renal impairment due to prolonged neuromuscular blockade.

Clinical use has diminished with the advent of newer nondepolarizing agents that have more predictable onset and duration and fewer histamine-related adverse effects. When reversal of blockade is required, acetylcholinesterase inhibitors such as neostigmine (often given with an antimuscarinic agent to counter muscarinic effects) or other reversal strategies are employed.

d-tubocurarine remains a historical benchmark in the development of modern neuromuscular blocking drugs and is largely of historical or limited use in contemporary practice.