전격경련(電擊痙攣)이 가토 혈당량에 미치는 영향

Abstract

[한글]

[영문]

Since electroshock treatment was first introcuced by Cerletti and Bini (1938) in psychiatric therapy, this treatment has been shown to have adventages over other convulsive treatments with respect to simplicity of the technique, side effects and hazard etc. Concerning the therapeutic efficacy numerous investigators have also reported that electroshock treatment amy favorably compare with insulin- and cardiazol-shock treatment. The curative mechanism, however, of the electroshock therapy is still obscure, and therefore, the knowledge of physiological changes during this treatment may eventually contribute to an understanding of this mechanism. Lee (1943) in our laboratory observed interesting changes in the blood picture of rabbits following electroshock : initial leucocytosis followed by leucopenia as as result of corresponding changes in lymphocytes and then later leucocytosis which was due to an increase in pseudoeosinophiles. By analyzing

various possibilities concerning this mechanism, be indicated that the activation of the symphatoadrenal system plays and important role in producing such changes in the leucocyte count. In the following studies, attempts have been made to determine the effect of electroshock on the blood sugar level in the rabbit and then to elucidate the mechanism by which the observed blood sugar response is controlled.

The electroshock convulsion was produced by the application of two electrodes on both sides of the head corresponding to the frontal motor areas. The electrodes were connected to alternating currents of 30-100 Volts with the duration of 2-10 seconds (approximately 100-300 mAmo.). Blood samples were drawn from ear veins at various time intervals after the electroshock and the concentration of blood sugar was determined by the procedure described by Hagedorn-Jonsen.

Result.

1. The electroshock convulsion was followed by a sudden rise in the concentration of blood sugar, reaching the maximum value within 30 minutes. The intensity of this blood sugar response varied from 16 per cent to 83 per cent, averaging 38 per cent

of the control level. This hyperglycemia returned to the normal level within two hours.

2. Bilateral vagotomy or prior administration of atropine did not influence the hyperglycemia induced by electroshock but rather tended to potentiate it in certain cases. This result nay indicate that the parasympathetic nervous system is not involved, neither centrally nor perinherally, in producing the hyperglycemia following electroshock.

3. Bilateral splanchnicotomy or prior administration of yohimbine markedly inhibited or blocked the blood sugar response to electroshock, indication that the sympathetic nervous system plays an important role in producing the hyperglycemia following electroshock.

4. A small dose of urethane (0.5 gm/kg) or of chloral hydrate (0.1 gm/kg), which usually produces a slight increase in the blood sugar level within 30-60 minutes, hardly affected the hyperglymia following electroshock. However, larger doses of these depressants markedly inhibited the intensity of the convulsion as well as the hyperglycemia caused by electroshock.

5. In the bilaterally adrenalectomized rabbits, the electroshock convulsion produced no effects on the blood sugar level.

6. The intravenous administration of 10 per cent cardiazol (0.15-0.40 ml/kg) produced a similar epileptiform convulsion and the hyperglycemia as those observed in the electroshock convulsion.

7. The intravenous administration of picrotoxin (1.0-1.5 mg/kg) resulted in a convulsion and a marked rise in the blood sugar level, reaching the maximum value within 1-2 hours.

8. The intravenous administration of strychnine nitrate (0.18-0.25 mg/kg) resulted in a tonic convulsion and opisthotonus within 5 minutes. A marked typerglycemia was also produced within 30 minutes after the convulsion.

From the above results it may be concluded that the blood sugar response to electroshock is mediated centrally through the sympatho-adrenal system. It has been clearly demonstrated in this experiment that the presence of the adrena lgland is necessary to produce hyperglycemia by electroshock, although further experiments will be required to determine whether the observed hyperglycemia is dependent on an increased secretion of the cortical hormone or the medullary hormone of the adrenal gland. In this experiment, it is difficult to differentiate the hyperglycemia caused by the electroshock convulsion form those caused by the cardiazol-, picrotoxin- and strychnine-convulsion. In view of the fact that the above convulsive agents produce hyperglycemia, presumably by affecting centrally the sympathetic nervous system (Tatum, 1940 ; Shirodo, 1941 ; Shismidoku, 1932), it is assumed that the blood sugar responses to electroshock and also to the convulsive agents may be controlled by similar mechanism(s).