The electrocorticographic responses in normal rabbits induced by injection of antihypertensive drugs were observed and the relationships of them to the reduction of the blood pressure were studied. Results: Slow waves were observed temporarily in the electrocorticogram from a obstructed side of hemispheres when a unilateral common carotid artery was obstructed and extreme dosis of the antihypertensive drug (above 50mg of Methobromin intravenously or above 30mg of Ansolysen intramuscularly) was injected in the rabbit. These slow waves did not necessarily appear in the maximal reduction of the blood pressure, but appeared already on the way of the reduction. Among them, slow waves were observed only on the way of reduction of the blood pressure and disappeared already when the blood pressure reached the maximal level of the reduction by intramuscular injection of 30mg of Ansolysen. The slow waves could not be observed in the electrocorticogram of the rabbit in which small dosis of the antihypertensive drug was injected or of the rabbit whose common carotid artery of any side was not obstructed. In a case of the rabbit whose common carotid artery of one side was obstructed, slow wave did not appear and only low voltage resulted when the blood pressure dropped abruptly and extremely after intravenous injection of 100mg of Methobromin. This rabbit succumbed to death after these observations. The duration of the appearance of the slow wave was long when the blood pressure rapidly dropped by intravenous injection of Methobromin, but that was short when the blood pressure slowly decreased by intramuscular injection of Ansolysen. From these results, it was supposed that compensatory mechanism of the cerebral vessels is present undoubtly and that decompensation of this mechanism is represented by the appearance of the slow wave in the electroencephalogram. And it was supposed that for the appearance of the slow wave after the injection of the antihypertensive drug, obstruction of the cerebral vessels, individual reactive attitude toward the antihypertensive drug, and speed and degree of decline of the blood pressure may be responsible.
This report deals with how capillary wall holds its normal strength. Several bioflavonoids which work as capillary stabilizer were selected and the mechanism of their actions were investigated. By inhibiting the formation of vasodilating substance like acetylcholine and histamine, capillary resistance can be increased. Therefore in this report, the correlation between 1-histidine decarboxylase (H.D.) and bioflavonoid has been investigated. Clostridium Perfringens PB 6K was used as H.D., because I have found previously that it had strong histamine-forming enzyme. Ascorbic acid has shown the strongest inhibition rate against H.D. among capillary stabilizer and its use with bioflavonoid increased its effect largely and the same effect on capillary resistance was observed also in clinical application. Myricitrin and myricetin have had stronger inhibitory action than others and Rutin and quercetin have shown almost the same effect. Cortisone, ACTH, AC-17 and Parotin have been found to have no inhibitory action against it. β-diethylaminoethyl-myricitrin has shown nice effect upon capillary wall. The fact that the clinical effect of bioflavonoid is parallel with its H.D. inhibition rate suggests that such mechanism is held also in vivo.
The agglutinogen titer of the erythrocyte was estimated in pulmonary tuberculosis patients and the healthy, and was investigated as to the relation to the grade of tuberculosis or to each sign of tuberculosis. The A-blood group serum as the agglutinin against the B-agglutinogen was obtained from a fixed healthy man normal in x-photo and blood sedimentation rate and positive in tuberculin reaction. The same was the case with the B-blood group serum. These standard sera were used for the agglutination reaction immediately after their preparation. The old sera were not used. The erythrocyte suspension of the patients to be tested was prepared by centrifuging their citrate blood and then by washing the obtained erythrocyte three times with a buffer. This suspension was dropped by one drop into a series of the gradually diluted solutions of the standard serum mentioned above, respectively. The agglutination was observed after 2 hours lapsed in an incubator. Thus, the agglutinogen titer was measured in 178 A-blood group patients, 150 B-group ones and 45 AB-group ones, and in 88 A-group healthy bodies, 59 B-group ones and 25 AB-group ones. In the A-and AB-blood groups, the A-agglutinogen titer under 25 was found more in incidence in the tuberculous than in the healthy. In the B-blood group, the B-agglutinogen titer under 25 or 27 was also found more in incidence in the tuberculous. But there was no distribution difference of the B-agglutinogen titer in the AB-blood group between the tuberculous and the healthy. Generally speaking, the agglutinogen titer in any blood group in lower in the tuberculous than in the healthy. Considering the blood sedimentation rate, x-photo, tubercle bacillus in sputum or gastric juice and complication, the patients were divided into three categories, namely the slight, moderate and severe. In the B-blood group, the B-agglutinogen titer under 25 was found the most in incidence in the severe category, and more in the moderate and less in the slight. It is well known that the serum of the tuberculous patients is abnormal. It, for instance, contains the antibody against tuberculosis, but it is not so discussed about the abnormality of the erythrocyte in tuberculosis. According to my experiment, the erythrocyte is as abnormal as to the agglutinogen titer as the serum as to the antibody in pulmonary tuberculosis.