other cleaned plant parts, and occasionally snake venom is boiled in water for two days. This liquid is then strained and evaporated to create a dark, heavy, viscid paste that would be tested for its potency later. This curare paste was described to be very bitter in taste. In 1938, Richard Gill and his expedition collected samples of processed curare and described its method of traditional preparation; one of the plant species used at that time was Chondrodendron tomentosum. Adjuvants Various irritating herbs, stinging insects, poisonous worms, and various parts of amphibians and reptiles are added to the preparation. Some of these accelerate the onset of action or increase the toxicity; others prevent the wound from healing or blood from coagulating. Diagnosis and management of curare poisoning Curare poisoning can be indicated by typical signs of neuromuscular-blocking drugs such as paralysis including respiration but not directly affecting the heart. Curare poisoning can be managed by artificial respiration such as mouth-to-mouth resuscitation. In a study of 29 army volunteers that were paralyzed with curare, artificial respiration managed to keep an oxygen saturation of always above 85%, a level at which there is no evidence of altered state of consciousness. Yet, curare poisoning mimics the total locked-in syndrome in that there is paralysis of every voluntarily controlled muscle in the body (including the eyes), making it practically impossible for the victim to confirm consciousness while paralyzed. Spontaneous breathing is resumed after the end of the duration of action of curare, which is generally between 30 minutes and 8 hours, depending on the variant of the toxin and dosage. Cardiac muscle is not directly affected by curare, but if more than four to six minutes has passed since respiratory cessation the cardiac muscle may stop functioning by oxygen-deprivation, making cardiopulmonary resuscitation including chest compressions necessary. Chemical antidote Since tubocurarine and the other components of curare bind reversibly to the ACh receptors, treatment for curare poisoning involves adding an acetylcholinesterase (AChE) inhibitor, which will stop the destruction of acetylcholine so that it can compete with curare. This can be done by administration of acetylcholinesterase (AChE) inhibitors such as pyridostigmine, neostigmine, physostigmine, and edrophonium. Acetylcholinesterase is an enzyme used to break down the acetylcholine (ACh) neurotransmitter left over in motor neuron synapses. The aforementioned inhibitors, termed "anticurare" drugs, reversibly bind to the enzyme's active site, prohibiting its ability to bind to its original target, ACh.