With the use of unrestrained and unanesthetized cats implanted with electrodes the author observed normal EEG as well as that of the cats under insulin-hypoglycemia. In addition, observations were carried on the influences of some drugs and electrical stimulation on hypoglycemic EEG. The results are as follows.
1. The low voltage fast waves observable in awaking state change to characteristic sleep spindle of about 12 c/s as the cat falls into sleeping state, and in deeper sleeping state high voltage slow waves appear in the cortex aud varlous nuclei of subcortex.
2. Hypoglycemic state was classified into lethargic, preconvulsive, convulsive and comatose stages on the basis of characteristic behavior, blood-sugar level and EEG.
In the lethargic stage, normal EEG from awaking to deep sleeping state appeared in all leads.
In the preconvulsive stage, disturbances of sympathetic nervous system and large slow wave burst were characteristic.
In the convulsive stage, spikes and sharp waves were predominant, and furthermore, myoclonic jerk in all muscles and occasionally general convulsion broke out suddenly.
In the comatose stage, cats were completely relaxed and l cycle/sec or less large slow waves appeared on EEG. In this instance when hypoglycemia was in progress, voltage diminished lower and lower.
3. Arousal effect of excitatory agents and amino acids on insulinhypoglycemia in comparison with that of glucose
a) General convulsion
Only when general convulsion was induced by electrical stimulation, metrazol and megimide, there could be observed hyperglycemia, awaking patterns on EEG and behavioral wakefulness. In comparison with glucose, however, arousal effect was transient and uncertain.
b) Amino acids
Sodium glutamate next to glucose had hyperglycemic and arousal action on hypoglycemic cats, but its action was not so fast and long as glucose. The greater the dosage of sodium glutamate administered, the more certain was the effect. Fast administration of Iarge dose, however, is dangerous because it is apt to induce general convulsion.
GABA (gamma-amino butyric acid) showed transient hyperglycemic action and aroušal patterns on EEG, but no essential change took place in behavior.
Although GABOB (gamma-amino beta-hydroxybutyric acid) was administered in the convulsive stage, no definite action was seen.
4. Administration of inhibitory agents to insulin-hypoglycemia
a) Nembutal
Nembutal administered intravenously in the convulsive stage caused spikes and sharp waves on EEG to disappear and then elicited spindle burst. While myoclonic seizures and convulsions were being suppressed, hypoglycemia continued to progress. In the comatose stage Nembutal was non-effective.
b) Chlorpromazine (Cp)
Although not so effective as Nembutal, an optimal dose of Cp allows hypoglycemia to proceed gradually. Precaution is necessary with this drug because, when a large dose of Cp is injected rapidly into vein in the convulsive state, it is apt to induce convulsion and then the animal cannot be aroused even by administration of glucose.
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