The effects of adrenaline on the volume of the liver and the portal pressure were studied. All experiments were carried out on dogs under urethane anaesthesia. The changes of the carotid blood pressure, the portal pressure, the blood pressure in the thoracic vena cava and of the volume of the liver were recorded on a photographic kymograph, and in this way were obtained the following results. 1) The changes in hapatic volume occurred simultaneously with the rise of arterial pressure: when 1 : 10000 solution of adrenaline was injected into the portal vein, the hepatic volume decreased to maximal degrees at the peaks of the rising arterial pressure (Fig. 2), and when adrenaline was injected into the femoral vein, the maximal decrease in hepatic volume occurred in the lowest stage of arterial pressure (Fig. 1) 2) The change in portal pressure was not parrallel to the change in hepatic volume. In systemic venous injection of adrenaline, an initial rise and secondary rise of portal pressure occured. (Fig. 1). In portal in jections, one marked rise in portal pressure was observed (Fig. 2), but after the occlusion of the hepatic artery, the primary and secondary rises in portal pressure were also observed by portal injection as shown in Fig. 3, B. 3) It is known from the following experiment that the chief cause of a rise in the portal pressure under adrenaline does not depend only upon the contraction of the hepatic blood vessels. The experiment employing Eck's fistula proved that the primary and secondary rises of portal pressure by injection of adrenaline were present even though there was no accompanying slow heart beat. (Fig.4, A and B) 4) The initial rise in portal pressure was due to the constrkction of the hepatic blood vessels plus the secondary dffects of the rise in arterial pressure. The secondary rise of portal pressure may be attributed to the constriction of the hepatic blood vessels plus the increased inflow in the portal system. 5) The blood flow in the hepatic artery is related to the maintenance of the portal pressure. When hepatic artery is occluded, the initial rise in portal pressure by injection of adrenaline was followed by a marked fall of the portal pressure (Fig. 3, A and B).

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In clinical diagnosis of ventricular hypertrophy, bundle branch brock, premature heart beat, tricuspidal- and aortic valvular insufficiency, it is of great significance to determine the time of arrival of activation in ECG. However, there still remains a contraversy as to the point indication it. For example, the onset of ingrinsic or intrinsicoid deflection is regarded as the point marking this by Lewis, Wilson in early stage and many other authors, while the end of this deflection is considered to mark it by Wilson. This report was made to elucidate the accurate relationship between it and intrinsicoid deflection. According to our results in calculation, the actual instant of arrival of activation could be reperesented by cross point of tracing with zero-line when the equivalent double layer, perpendicular to the ling axis of straight muscle strip, was moved from one end to another. The time interval between the onset of the int. defl. and the cross point was variablw according to the transmission rate of activation and the distance from electode to muscle strip. When the equivalent double layer, oblique to hte long axis of the muscle strip,w was moved from one end to another, it could not be reperesented by cross point, differing from above mentioned case. Consequently, the onset of intrinsicoid deflection or the cross point of this deflection with zero-line could not be regarded as the representative point of arrival of activation even in simple activation process like above mentioned cases. Since the activation process in human heart is notso simple as that applying to above cases, we want to calculate the potential variation arising in more complicated activation process. When we calculated the potential change at a given point without a hollow polaraized sphoere in a certain process of activation, the time of arrival of activation was somewhre within the duration of intrinsicoid deflection. Moreover, when we calculated the potential variation at many points without heart in a feew process og activation, the arrival of activation occurred some where during the intrinsicoid deflection and was not upon a specific point like the onset or the end of the deflection. These caliculations were made on the schema of heart quoted from the atlas of anatomy by Toldt Hochstetter, assuming the every equivalent double layer in each stadium of activation as a disk. It must be noted that the intrinsicoid deflection is not necessarily sharp and large deflection but sometimes smaller than the deflection due to the extrinsic effect, and it is not always easy to point out the intrinsicoid deflection in ECG. Comparing these results of calculation with those of experiments pwerformed on toad heart, recording the contiguous bipolar lead ECG and unipolar lead ECG simultaneously, we could observe that the both results coincident very well. We may conclude that the onset or the end ofthe intrinsicoid deflection can not be interpreted as the point indicating the arrival of activation as Lewis Wilson and others say, and that ingrinsicoid deflection is not neccessarily a large and sharp deflection but sometimes smaller then the deflection due to extrinsic effect. In general, the time of arrival of activation lies somewhere during the intrinsicoid deflection, bu can not be defined on a specific point.

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Using rabbits the author succeeded in producing congestive heart failure by loading them with NaCl in addition to experimental institution of aortic of pulmonary stenosis and allergic myocatditis. Changes of circulating blood volume in such conditions were investigated using dye T-1824. It was shown that it dimnished as hemodynamical disturbance of heart developed. This fact does not mean the diminution of the whole blood volume.

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I studied Whether myoglodin (to de abbreviated hereafter to mb)-antibodies in rice-illness causes allergic changes in catdiac tissue and the other organs. Furthermore, I investigated pathologic-histologically the relation of this phenomenon to the pathogenesis of so-called beriberi heart. This experiment consists of two groups. I group employinf antichickness mb (in rice-illness) rabbit immune serum, II group being sensitized over and over agein with chickness mb in rice-illness. Results obtained are summarized in the following. I group:- Speaking of heart treated, the allergic myocarditis occarred in all cases, especially with perivascular or interstitial cell-infiltration, fibrinoid degeneration of wall of blood vessels and degeneration of heart muscles. On the other hand, interstitial cell-infiltration in liver, proliferation of interstitium, swelling or desq-u amation of epithelium of tuble and proliferation of gromelurus epithelium in kidney, and perivascular cell infiltration in sceletal muscles etc. were also observed. But the group treated with myosin and myogen showed slight pathological changes.

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Since the first report by Schellong. in 1936, many researches have been done by many authors on vectorial method of electrical heart events Because of excellency of this method for researches of cardiac function or for diagnosis of heart diseases, various methods have been developed. Among of them, the Polyography by Toyoshima. is the most excellent method so far as they concern with vectorial representation with scarce deformation. But, for the reason of its requirement of a special Braun tube, we can not apply it easily anywhere. So another new simple and excellent method of vectorcardiography was reported here. This is one of the type of multipolar chest lead VCG like polygraphy by Toyoshima. To obtain the spatial VCG, four pairs of electrodes were placed on the chest wall surroundings the heart circularly. The position of electrodes in frontal, horizontal and sagittal VCG were the same with those by Polyography. In this method it was sufficient to only two push-pull amplifiers instead of four push-pull amplifiers by Polyography, because four electrodes situating opposite to each other were used as a pair of in-put electrodes being connected to one terminal through each 100,000 ohm resistance. Namely the in-put voltage in vertical or horizontal lead was led from each four electrodes situating opposite up to down or side to side. According to the previous reports by Toyoshima. and co-workers, vectors obtained by calculations were almost identical to those by experiments. The sa,e fact was recognized also in these model experimens. So the discrepancy represented vector was discussed by calculation. The result were follows. The VCG obtained by this method showed far less deformation than those by usual method and was not so different from polyograms. The excellency of this method was proved more distinctly by the excentrical position of generating electromotive forces. Further, here was discussed also the deformation of VCG obtained by eight pairs of electrodes instead of four pairs. The VCG by eight pairs showed less deformation than those by four pairs. It may be expected farless deformation when used 16,32 ... pairs of electrodes. The more electrodes were used, the less deformation could be recognized. Supplementally, here was discussed the deformation of VCG by nearly same method. in which single ended amplifiers were used instead of push-pull ones. By this method larger deformation could be recognized than that by push-pull amplifiers. If there was any short circuit between the vertical and horizontal deflection plates, it was indispensable to change push-pull connection to single ended ones in its last stage. The characteristics of this new method were as follows. 1) The more electrodes were used, the less deformation could be recognized. 2) However numerous the electrodes might be , it was sufficient to use only two push-pull amplifiers. 3) it did not require a special Braun tube for this new method, but could be dealed sufficiently with an usual Braun tube.

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