In spite of considerable clinical and experimental work, the physiologic activities involved in sweating produced by pilocarpine and mecholyl (acetylbetamethylcholine hydrochloride) are not completely understood. In 1931 Cushing1 suggested that pilocarpine may act centrally on a parasympathetic center in the diencephalon. He produced in man by intraventricular injection of pilocarpine (and also of extract of posterior pituitary) generalized vasodilation, sweating, decrease in temperature, salivation and vomiting. This reaction was not obtained in patients in whom the hypothalamic area was destroyed (by tumor).
Cushing's statement was not in agreement with the experience of previous investigators, who maintained that pilocarpine when administered subcutaneously had a peripheral point of attack. Langley,2 Langley and Anderson,3 Burn4 and Wilson5 assumed that pilocarpine acted directly on the sweat glands. These authors supported their view by the fact that the response to pilocarpine is preserved after degeneration of the postganglionic sympathetic fibers,