In regard to the determinant molecular group of antigen in allegic reactions, Prof. Dr. MAEKAWA pointed out the phosphatide, especially cephalin-fraction as its determinant one on the basis of experimental "Erythron-Allergy". In this report, in order to study the problem in the determinant molecular group of antigen in the experimental myocarditis caused with myocardium phosphatide the author extracted two fractions, from the myocardium phosphatide.i.e., cephalin- and lecithinfraction In cephalin group, consisted of 3 rabbits, the mixture of cephalin (1∼3mg) and bovine serum (2ml per kg of body weight) were injected seven times every other day, and in lecithin group, consisted of 4 rabbits with the mixture of lecithin (10mg) and bovine serum (2ml per kg of body weight) in the same way. Seven days after the last injection they were killed, and their organs were investigated histologically.Clinically body weight and urine were unchanged. In cephalin group lymphocytes decreased at the beginning of the sensitization and then increased, in their hemograms shift to the left and appearance of young cells of myelocytic series were observed. In both groups their serum protein level especially gumma globulin fraction increased, but this increase had no relation to the histological changes of their heart. One rabbit serum in cephalin group showed T-peak electrophoretically.The allergic changes of all rabbits in cephalin group were remarkable, i.e., the panarteriitis from middle big arteries to arterioles were found. Intima and media of coronary arteries hypertrophied and the intimagranuloma were found, thereby the cavity became narrow or closed entirely. The cell infiltrations, chiefly consisted of plasma cell, were found around the coronary arteries and in the perivascular myocardium. These findings were similar to the allergic granuloma by KLINGE. On the contrary in lecithin group only two of four rabbits showed these changes in their heart, however, these changes were slighter than those three in cephalin group. Lung, liver, spleen were unchanged but in a few rabbits in both groups inspecific nephritis occurred.There were no essential difference between my result with bovine myocardium cephalin, NODA's result caused with rabbit myocardium phosphatide and ARAKI and MORISAWA's result caused with human myocardium phosphatide, therefore, the myocardium cephalin has no species-specificity.Consideration of the results reported above lead me to the conclusion that the myocardium cephalin is the determinant molecular group of antigen among the myocardium phosphatide.

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In order to investigate mechanism of phlorizin action, there were observed effects of a single intravenous administration of this drug on renal clearances in man and rabbits. Simultaneous thiosulfate, endogenous creatinine, glucose and PAH clearances in man were measured by means of the simplified method, and exogenous creatinine clearance and glucose Tm in rabbits were measured by the continuous intravenous infusion of creatinine and glucose solution. Results are as follows : 1) The administration of phlorizin in man causes a marked reduction in endogenous creatinine, thiosulfate and PAH clearances, above all the more marked reduction in PAH clearance as against other clearances raises the filtration fraction. It gives a proof that phlorizin brings about renal circulatory disturbances, presumably accompanying secondary reduction in thiosulfate and endogenous creatinine clearances.2) The intravenous administration of phlorizin in adequate doses enables to raise the glucose/endogenous creatinine clearance ratio to 1.0; and the minimum intravenous dose of phlorizin required in the normal man to raise the glucose clearance to thiosulfate or endogenous creatinine clearance was found to be in the neighbourhood of 10mg. per kg. body weight, and this dose not show significant deviation between the normal and the renal diseases or hypertension. This fact is interpreted as indicating that phlorizin may paralyze completely the tubular reabsorption of glucose.3) It may be noted that exogenous creatinine clearance and glucose Tm decreased in phlorizinized rabbits, and that especially glucose Tm dropped from an average value of 28.52mg/min to about 0 after the administration of large dose of this drug (above 119mg. per kg. body weight). This demonstrates the complete inhibition of the tubular reabsorption of glucose.4) The thiosulfate/endogenous creatinine clearance ratio was not affected appreciably after phlorizination in the normal, renal diseases and hypertension.5) For the increase of urine flow and the decrease of RR (water reabsorption) after administration of this drug, it seems due to chiefly osmotic action offered by gluose in tubular urine and perhaps partly depressive action on the water rebsorptive function of phlorizin per se.6) It is reacognized that phlorizin dose not affect appreciably blood pressure in the normal, renal disease and hypertension.7) There were no objective or subjective unfavorable reactions after the intravenous administration of phlorizin in the normal man, but the increase of oedema and the decrease of urine flow were observed temporarily in a few of the nephrotic syndrome.In conclusion, it is confirmed that the intravenous administration of phlorizin depresses the tubule reabsorption of glucose and its large dose enables the complete inhibition. The renal circulatory disturbances caused by phlorizin bring about marked reduction in all renal clearances, and the accompanying diuresis is due to mostly osmotic action offered by glucose in tubular urine and partly taking part in depressive action on the water reabsorptive function of phlorizin per se.

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It has been found by Toyoshima and ramada that when the activation process of human heart ventricle was known, the ECG and VCG could be reconstructed from their tables of potential calculation, in which the potentials of ventricular unit areas were obtained by measuring the solid angle at many lead points of ECG and VCG.So, I tried the analysis of the electrocardiographic and vectorcardiographic changes in the ventricular hypertrophy by means of reconstruction of ECG and VCG under the next three conditions.First condition : Enlargement of the ventricular surface of either side. Second condition : Delay of activation of subepicardial muscle in hypertrophied ventricular wall. Third condition : Combined condition of the first and second one. Under the first condition, I could obtain ECG and VCG resembled closely in configuration to those practically recorded from patients with ventricular hypertrophy. I found also that the earlier onset of intrinsicoid deflection in V₁ and V₂ in the left ventricular hypertrophy, which was described in the text book of ECG by Hecht, could be attributed to the effect of dilated left ventricular endocardium. Under the second condition, I could obtain ECG and VCG resembled in configuration to those in ventricular hypertrophy, too, but I could find neither enlargement of QRS-complex nor earlier onset of intrinsicoid deflection in V₁ and V₂ in the left ventricular hypertrophy. Under the third condition, I could obtain the most resembled ECG and VCG to those in hypertrophy and could find also the enlargement of QRS-complex and the earlier onset of intrinsicoid deflection in V₁ and V₂ in left ventricular hypertrophy. In some cases of right ventricular hypertrophy, the QRS-loop was inscribed in a contrary direction to the normal in the horizontal and sagittal plane. Under any condition of these three, especially under the third condition, the middle portion of QRS-loop was displaced to the left-posterior in the left ventricular hypertrophy and to the right-anterior in the right ventricular hypertrophy. In the right ventricular hypertrophy, the R-wave in right precordial lead became large and the S-wave in left precordial lead became deep. In the left ventricular hypertrophy, the R-wave in right precordial lead and the S-wave in left procordial lead became small and V₁ and V₂ were often inscribed with QS-wave, but the S-wave in right precordial lead and the R-wave in left precordial lead became large. From these findings in reconstruction of ECG and VCG, I could find that the cause of characteristic changes of ECG and VCG in the ventricular hypertrophy could be attributed not only to the rotation of the heart around its long axis but also to the dilatation of ventricle or the delay of the arrival of the activation in the subepicardial muscle of the hypertrophied ventricular wall.

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There are many reports in which the ECG were exlained by the change of solid angle at point to lead subtended by the activated ventricular area, but no one has ever discussed the ECG measuring actually the solid angle at that point. Toyoshima and associate reported previously that ECG and VCG could be reconstructed from their results of potential calculation, when the ventricular activation process were known. So, I attempted the reconstruction of ECG and VCG by their method under various assumptive activation processes dividing them into eight stages. Since the potential calculation having been done only on epicardial surface of plaster model of human heart, the potential due to septal activation could not be obtained. But the effect of septal activation may not be large because of almost the same onset of septal activation in both side. The potential due to endocardial surface was assumed as one half of those due to the corresponding epicardial surface in the first depolarization stages. In the sequent stages, I assumed those potentials as 0.7 to 0.8 times of latter, and in the last stafe of subendocardial depolarization as the same with latter.The method of reconstruction of VCG and ECG. The potentials at the leading points by cube system method and polyography were obtained by calculation in each stage of depolarization. From these calculative potentials, the manifest vectors were reconstructed geometrically, and the VCG were recorded by plotting the ends of these vectors. Standard limb lead ECG were obtained from potential difference between the representative points of extremities. Unipolar lead ECGs were obtained by subtracting one third of the sum of three extremity potentials from their potentials.ECG and VCG thus obtained resembled closely to the usual ones, and the assumptive activation processes used for the reconstruction were not much differed from that by Lewis, by Harris and by Toyoshima. By this method, the relationship between the VCG or ECG and ventricular activation process of human heart could be ascertained more theoretically than usual methods, and the following facts could be also confirmed.1) It was desirable selecting the center of spatial vectorcardiographic reference system as near as possible to the cardiac center level, while the configuration of VCG was inscribed normally when the center of reference system was placed on the same level with cardiac center, and when it was displaced, the VCG was recorded in abnormal configuration. For example, when the leading points were selected higher as much as 10 cm than that, sagittal plane VCG was inscribed in contrary direction.2) Various electrical heart positions were found even from the same heart position, if the activation process were changed.3) Strictly speaking, unipolar precordial ECG were not scalar projection of horizontal plane QRS-loop of VCG in geometrical sense.4) The time of arrival of activation was marked at anywhere in the intrinsicoid deflection and not at the specific point of it.5) The typical configuration of the VCG and ECG of cor palmonale was obtained by increasing the area and delaying the activation stage of concerning heart region. It was suggested also that the ECG and spatial VCG of hypertrophy, bundle branch block, and myocardial infarction might be reconstructed in the same way.

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Author observed the influence of vitacampher, adrenalin and acetylcholine on respiration of rat's heart muscle slices, using the same method described in Part III of this article. As substrate 0.01 M glucose and as gas pure oxygen was used.Results were as follows.1) Vitacampher depressed respiration markedly. It was more marked when vitacampher-concentration was higher. (Table I, Fig. 1)2) Adrenalin depressed respiration contrary to the experiment in vivo reported by many workers. This was more marked when adrenalin-concentration was higher, just as in vitacampher experiment.(Table II, Fig 2)3) Acetylcholine had reverse action on respiration, namely accelerated respiration. Then this too, was contrary to the experiment in vivo. But in higher concentration of acetylcholine it was depressive. (Table III, Eig. 2) 4) It was found that cardiac glycosides about which action was described in another report No. 3, vitacampher, adren alin and acetylcoline, all showed similar depressive action in their higher concentration.

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