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Curare is the generic term for the resinous arrowhead poisons used to paralyze hunted animals.116 The curare alkaloids are derived from the bark of the Strychnos vine, and the most potent alkaloids, the toxiferines, are derived from Strychnos toxifera. Fortunately for the hunters who used curare, ingestion of their prey did not cause paralysis. Sir Walter Raleigh discovered the use of curare in Guyana in 1595, and he was the first person to bring curare to Europe. Curare played a pivotal role in the discovery of the mechanism of neuromuscular transmission. In 1844, Claude Bernard placed a small piece of dry curare under the skin of a live frog and observed that the frog became limp and died.8 He performed an immediate autopsy and discovered that the heart was beating. Because direct muscle stimulation produced contraction but nerve stimulation did not, Bernard concluded that curare paralyzed the motor nerves. He later observed, however, that bathing the isolated nerve did not affect neuromuscular transmission, leading him to conclude: “Curare must act on the terminal plates of motor nerves.”18 Curare was used by Nobel Laureate physiologists Charles Sherrington, John Eccles, and ­Bernard Katz to further elucidate neuromuscular physiology. Its first clinical use was described in 1878 when Hunter used curare to treat patients with tetanus and seizures.116 In 1932, Raynard West used curare to reduce the muscular rigidity of hemiplegia.116

Curare (d-tubocurarine) was introduced into clinical anesthesia in 1943 by Harold Griffith and Enid Johnson.43 Endotracheal intubation during general anesthesia was not common those days, so d-tubocurarine was administered in a dose that spared the diaphragm and maintained spontaneous ventilation. It was not until 1954 when Henry Beecher found that patients receiving d-tubocurarine had a sixfold increase in respiratory-related anesthesia mortality that artificial ventilation and reversal of residual d-­tubocurarine became a routine practice.9 Use of d-tubocurarine spanned almost 40 years until it was replaced by superior nondepolarizing neuromuscular blockers that caused less histamine release and hypotension.

Around the same time in the 1950s that curare gained popularity in the operating room, succinylcholine also came to clinical use to facilitate orotracheal intubation.9 In the nonmedical world, succinylcholine carried a reputation of being the “person poison.”3 This came to media attention when a high-profile killing case involving an anesthesiologist Dr. Carl Coppolino and his mistress were accused of murdering his wife and the mistress’s husband in 1966 and 1967, respectively, by injecting succinylcholine.77 In 1983, shortly after Dr. Michael Swango began his internship at Ohio State University ­Hospital, patients began dying inexplicably, and he was relieved of his duties.109 Following switching residencies and jobs for 14 years, prosecutors secured Swango’s guilty plea for the murder of three victims. The toxicological analysis of the 7-year-old remains of Thomas Sammarco revealed succinylcholine in the liver and gallbladder and its metabolite succinylmonocholine in multiple organs, which assisted in ...

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