Читать книгу From Poison Arrows to Prozac - Stanley Feldman - Страница 16

One of the problems that dogged the early experiments with the South American arrow poison was the variation that occurred in the amounts of the different ingredients that went into the samples used and the question of whether it deteriorated with age. Benjamin Brodie recognised this and commented that his woorari was similar to that supplied to the Abbé Fontana for his experiments.

The poison certainly varied according to the region in which it was produced. Specimens collected from the Orinoco basin by the Schomburgks were largely composed of the bark and root of the creeper Strychnos nux. (Fig 7) Indeed, they called the poison Strychnos toxifera. As a result of its strychnine content, the immediate convulsive effects predominated, concealing the onset of the paralysis produced by the curare. This was probably why the German physiologist Albert von Bezold, using a preparation given to him by the Schombergs, believed the drug killed its victims by inducing convulsions. The poisons prepared from the more western jungles of Ecuador and the Peru were principally composed of an extract of the bark of vicuñas, and particularly that of the creeper, Chondrodendron tomentosum. (Fig 8) These contained high concentrations of curare and were similar to those collected by Waterton and those used by Brodie to demonstrate the paralytic properties possessed by their toxins. In an attempt to reduce the confusion, Dr Rudolph Boehm, in 1886, suggested classifying the curares according to their mode of preparation in the belief that the means used to store the poison indicated the region from which it came. He separated the curares into pot curare, tube curare, and calabash or gourd curare. This classification reduced the confusion, but it was not until 1935 – when Harold King, working in the Burroughs Wellcome laboratories in England, isolated and identified the chemical structure of curare – that pure specimens of the drug became available for study.

By the middle of the nineteenth century supplies of crude tube and calabash curare, of a reasonably consistent quality, were available in Europe thanks to the work of Wilhelm Peyer, who prepared a crystalline salt of the poison. Although this was later shown to contain potassium carbonate and phosphate as impurities, it was much better than the crude preparations previously available.

By this time it was appreciated that curare caused death by paralysing the muscles of ventilation, and that, provided artificial ventilation was maintained, it did not cause any long-lasting ill effect on the body. The riddle of how and why it produced paralysis was to wait until the simple, elegant experiments of Claude Bernard in France, the intuition of the physiologist Otto Loewi and the experiments of the Henry (later Sir Henry) Dale and his team of fellow pharmacologists at University College, London.