The electroencephalographic responses in 52 hypertensive subjects induced by injection of clinical dosis of antihypertensive drugs were observed and factors producing the electroencephalographic responses were studied. In 37 cases among 52 hypertensive subjects electroencephalographic responses were recognized after injection of the drugs and in 12 cases of them prominent responses were observed. The author investigated correlations between the electroencephalographic responses and various clinical findings. As a result, it was found that the electroencephalographic responses might be influe-enced by following factors: 1) initial systolic blood pressure, 2) initial diastolic blood pressure, 3) rate of decrease in the systolic blood pressure, 4) rate of decrease in the diastolic blood pressure, and 5) arteriosclerotic degree in retinal back ground. In the cases showing prominent electroencephalographic responses, marked disrhyth-mias and disorders in, the electroencephalogram like as the epileptic seizure patterns were observed in 4 cases, the paroxysmal slow wave bursts with or without spikes, in 7 cases, and the disappearance of slow wave bursts which were seen before the injection, in one case. Focal electroencephalographic responses in a wide sense were found in 4 cases. From these results, the administration of the antihypertensive drug, even though within its clinical dosis, may produce frequently the electroencephalographic responses suggesting cerebral vascular insufficiency in hypertensive subjects with high initial blood pressure and cerebral arteriosclerosis of high degree. Therefore, when antihypertensive drug is injected in hypertensive subject, special attention must be paid. The injection caused sometimes the symptoms alarming the dosage of antihypertensive drug, but if it is used carefully, it is harmless and may be useful for the determination of the focus in the brain and for the activation of electroencephalogram in epileptics.
Cysteine administered to normal rabbits showed a remarkable effect on leucocyte count with its two characteristic peaks in the increasing phase the first peak appeared three to four hours after the administration of cysteine, and the other six to eight hours after it. For the purpose of finding out by what mechanism the above peaks were formed, cysteine was administered to the rabbits with the cervical cord severed and those with the liver injured by CCl4, and the leucocyte increasing effect upon them was investigated as in the first report. The results obtained are as follows: 1. In the rabbits with the cervical cord severed the second leucocytosis did not appear and only the first one was observed. 2. In the rabbits with the liver injured by CCl4 just about the same leucocyte increasing effect was revealed as in the normal rabbits with two characteristic peaks of leucocytosis. Especially the first peak was remarkably proved in all cases. 3. Taking into consideration the results from the two experiments, it can be recognized that cysteine exerts both peripheral (working directly on the bone marrow) and indirect central action controlled by the central nervous system-the first peak being caused by the peripheral and the second by the central action.
The leucocytosis promoting effects have been studied by the administration of cysteine and typhoid vaccine (T.V.), a kind of typical centrally leucocyte increasing substance, to the rabbits with the hematopoietic organs injured by Nitromin. Cysteine and T.V. were administered at times when the above injury proved strongest and slight. The results obtained were as follows: 1. As in the case of the strongest injury, the promoting effects of cysteine and T.V. were weak and delayed. 2. As in the case of the strongest injury, the first peak of the two-peaked phase never appeared and the second one was remarkably delayed and low. The initial negative phenomenon by the injection of T.V. appeared irrespective of the degree of the injury, but in the case of the strongest injury, the duration of the phenomenon were prolonged. 3. As in the case of the slight injury, both cysteine and T.V. produced a regular marked promoting effect on the leucocyte count. 4. Since the injury of the leucocyte-storing organs was found slight even in the case of the strongest injury (of the hematopoietic organs), the leucocyte mobilizing action of cysteine was not by releasing the stored leucocytes. 5. When the hematopoietic organs were injured, the leucocyte increasing effect of T.V. was more noted than that of cysteine. This difference is induced by the temporary alteration of the periphere vessels and means that T.V. injection produces a marked retaining action on peripheral leucocytes.