Since acetylcholine has such great importance in the body it is not surprising that attempts have been made to use it in therapeutics. But a substance with such a huge variety of effects and so rapidly destroyed in the body is unlikely to be useful when given systemically, as its history in psychiatry illustrates.
Acetylcholine was first injected intravenously as a therapeutic convulsant in 1939, in the justified expectation that the fits would be less liable to cause fractures than those following therapeutic leptazol convulsions. Recovery rates of up to 80% were claimed in various psychotic conditions. Enthusiasm began to wane however when it was shown that the fits were due to anoxia resulting from cardiac arrest and not to pharmacological effects on the brain.1
The following description is illustrative:
A few seconds after the injection (which was given as rapidly as possible, to avoid total destruction in the blood) the patient sat up 'with knees drawn up to the chest, the arms flexed and the head bent forward. There were repeated violent coughs, sometimes with flushing. Forced swallowing and loud peristaltic rumblings could be heard'. Respiration was laboured and irregular. 'The coughing abated as the patient sank back in the bed. Forty seconds after the injection the radial and apical pulse were zero and the patient became comatose.' The pupils dilated, and deep reflexes were hyperactive. In 45 seconds the patient went into opisthotonos with brief apnoea. Lachrymation, sweating and borborygmi were prominent. The deep reflexes became diminished. The patient then relaxed and 'lay quietly in bed — cold moist and gray. In about 90 seconds, flushing of the face marked the return of the pulse'. The respiratory rate rose and consciousness returned in about 125 seconds. The patients sometimes micturated but did not defaecate. They 'tended to lie quietly in bed after the treatment'. 'Most of the patients were reluctant to be retreated'.2
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