Curare muscular effects

The local injection of 0.1 to 2% procaine or other anesthetics blocks the centripetal proprioceptive impulses and thereby relaxes muscular tonus, normal and abnormal, such as spasmodic torticollis. It effects almost instantaneous relief of the pain, stiffness, malposition, and incapacity of fibrositis, lumbago, and acute sprains and fractures. The site of greatest tenderness may be infiltrated with 10 to 30 cc of 1 or 2% procaine hydrochloride. Injected systemically, it relaxes traumatic tetanus and removes decerebrate rigidity, so that spontaneous movements of the limbs and of the respiration return. Its curare action may also be concerned in this effect. It relaxes parkinsonian, but not myotonic, rigidity. 

Early studies showed that curare blockade was increased by tetracychnes (71-73). This effect can be antagonized by calcium ions (74). There was a shortterm increase in muscular weakness in patients with myasthenia gravis after intravenous tetracycline. The mechanism may be a calcium-antagonizing effect of magnesium ions present in the tetracycline solvent, as the... 

It has been known for centuries that the material called curare has the effect of causing muscular paralysis. This material had been brought to Europe from South America in small quantities by explorers, and was known to have been prepared by the natives in the form of aqueous extracts and concentrates for use as arrow poisons. The early history of the South American Indian arrow poisons has been described in detail by McIntyre (1). The samples available for scientific examination have varied so widely in botanical origin, physiological potency, and chemical constitution that it is only in recent years that definite information has been obtained about the chemical compounds responsible for the curare activity of the South American curare. 

Coniine causes death by blocking the neuromuscular junction in a manner similar to curare this results in an ascending muscular paralysis with eventual paralysis of the respiratory muscles which results in death due to lack of oxygen to the heart and brain [80]. Death can be prevented by artificial ventilation until the effects have worn off 48-72 h later. For an adult, the ingestion of more than 100 mg of coniine (approximately 6-8 fresh leaves, or a smaller dose of the seeds or root) may be fatal [70, 85],... 

Langley applied nicotine to the frog s sartorius muscle by means of a fine brush. He observed a local contraction only when the drug was applied to the neural region of muscle fibre. The application of nicotine to other parts of the fibre were without effect The application of curare to the neural region of the fibre blocked both the effects of nerve stimulation and the effects of the nicotine but did not interfere with muscular contraction in response to direct stimulation. The application of drugs to the nerve was infective. The action of nicotine persisted after nerve de neration and curare stQl prevented it... 

Sporadic attempts were made during the nineteenth and early twentieth centuries to use curare for the treatment of certain conditions, principally rabies, tetanus, epilepsy and spastic paralysis, and chorea, where it seemed that the muscular relaxation brought about by the drug would have beneficial effects. But the rarity of the substance, the tremendous variation in its activity, and the inability to standardize the product prevented any widespread use (22, 27). However that may be, as early as 1912 Lawen used a sample of Boehm s curarine as an adjunct to anaesthesia, thus anticipating the work of Griffith and Johnson (below) by some 30 years. It is unfortunate that this pioneering effort never received due recognition (22 p. 110,485 pp. 135-136). 

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