Journal of Mental Science (1949) 95: 930-944. doi: 10.1192/bjp.95.401.930
© 1949 The Royal College of Psychiatrists
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The Action of Glutamic Acid in Hypoglycaemic Coma*

H. Weil-Malherbe

Runwell Hospital, Wickford, Essex

* A Paper read at the Quarterly Meeting of the Royal Medico-Psychological Association on 23 February, 1949.

ABSTRACT

The effects of intravenous injection of a 25 per cent. neutral solution of glutamic acid have been studied after the onset of hypoglycaemic coma in patients undergoing insulin shock therapy and the following observations are recorded:

  1. The minimum effective dose of glutamic acid solution necessary for the restoration of consciousness in comatose patients was found to be 5 ml., and in favourable cases 2 ml. The blood-sugar rise produced by these doses is greater than can be accounted for by the amount of glutamic acid injected. It is concluded that the effect is due neither to a direct utilization of glutamic acid as fuel for the brain cells nor to its conversion into glucose by the liver, and it is suggested that only a catalytic mechanism can account for the high degree of activity of glutamic acid.
  2. The injection of glutamic acid induced the classical triad of adrenaline action: a fleeting rise of blood pressure and pulse rate (the latter only when it was not accelerated before the injection) and a rise in blood sugar.
  3. Blood samples taken before and after the injection of glutamic acid were examined for adrenergic activity by the rabbit's intestine method. No effect was found when whole blood or plasma was tested, but when a solution of washed and laked blood corpuscles was used the post-injection sample frequently showed a clear increase of adrenergic activity over the pre-injection sample.
  4. Intravenous injection of adrenaline at the rate of 50 µgm./min. duplicated in every respect the effect of glutamic acid in terminating the coma and in producing a blood-sugar rise.
  5. Injection of "casydrol," a 5 per cent. enzymic digest of casein, in doses which contained more than twice as much amino-N as the minimum effective close of glutamic acid, had some effect on blood-pressure and blood sugar and in some cases lessened the depth of coma, but full restoration of consciousness was not observed. It is concluded that the effect of glutamic acid is not merely a function of its amino-N.

The results are discussed and the opinion is expressed that the objections against the adrenergic mechanism of the glutamic acid effect are without foundation. It is also suggested that an adrenergic mechanism may account for the favourable results of glutamic acid therapy in mental deficiency.