Introduction This work was performed based upon allergic focal infection and tuberculosis-allergic reaction in rheumatic disease and especially MAEKAWA's assertion about allergic organ-affinity. As antigen the human type tubercle bacilli with rabbit-myocardium-phosphatide, which has a manifest affinity for its myocardium and as focus the testicles of rabbit have been selected. By this way I intended to produce a high allergic myocarditis in sensitized rabbits. Method The rabbits used for the purpose were sesitized with the above-stated antigen in their both testicles in alternate side at every three day during three months and reinjected intravenously by the same antigen at the 10th day after the last (30th) sensitization and then dissected at the 7th day after the reinjection. For control another group of rabbits were sensitized and reinjected by the human type tubercle bacilli alone. During the full course of this experiment all rabbits were observed clinically, serologically and histologically.

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Many works have been already reported, by those which was confirmed MAEKAWA's Idea that the substance which determines allergic affinity must be cell phosphatide. As one of these works I sensitized the rabbits intravenously with a mixture of rabbit-lung-phosphatide and fresh oxen sera. At about three weeks after the sensitization these rabbits were reinjected by the same antigen and then dissected. During the total course of this experiment I examined each organ clinically, serologically and histologically.

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The diagnosis of origin of ventricular premature beat in ECG is not yet unified. So, I performed the experimental research on the diagnosis of origin of ventricular premature beat by polyography exciting the various points of toad heart with induction stimulator. Points of lead were selected eight point on the ventral surface surrounding the heart with same distance. In some cases the direct unipolar electrocardiograms were led from epicardial and endocardial surface adjacent to stimulated point to sompare with the results of VCGs. 1) The polyograms obtained by stimulation of the corresponding epicardial and endocardial surfaces were coincided very well in their forms, directions of long axesm initial and terminal directions and rotation of QRS. loops. These findings showed that the effect of the electromotive force across the ventricular wall at stimulated point was too small to change the vectorcardiogram. I ascertained also these findings by direct unipolar lead ECGs. Namely, when I stimulated the epicardial surface and led the unipolar ECG from adjacent point to it, the tracing began with Q wave after 0.01 sec. (mean value) of latency. Stimulated the endocardial surface mear the apex and led the unipolar ECG from just above points on epicardial surface the tracing began with Q wave after 0.07 sec (mean value) of latency. On the contrary, stimulated the epicardial surface and led the unipolar ECG from subjacent endocardial surface, the tracing began also with Q wave after 0.14 sec. (mean value) of latency. Both curves were resembled very closely each other except the latency. When the endocardial surface near the base was stimulated, the ECG began with alike wave to natural one and could not be used as a critical one. 2) The initial direction of QRS loop by artificial premature ventricular beat were coincident very well with direction of inward normal at stimulated point and not with that toward the center of gravity. The direction of long axis of QRS loop coincided also relatively well with that of inward normal. 3) The initial direction of QRS loops obtained by stimulation of basal endocardial surface differed relatively in wide range from direction of inward normal. The cause of discrepancy in their direction may be the entrance of stimuli in the funneleled normal conducting tissue in relatively eary stage. 4) The terminal direction of QRS loop coincided relatively well with the direction of outward normal and countercloolwise when the left lateral wall. 7) From these findings we could diagnose the origin of ventricular premature beat, but the differentiation of it whether it came from endocardium or epicardium was impossible.

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As the second group, chickens sensitized over and over again for a long time with chickens mb in rice-illness, and its pathologic-histological changes observed. The treated hearts showed the allergic myocarditis, expecially with perivascular cell-infiltration (lymphocytes, plasma cell, monocytes, eosinophiles and great basophilous mononuclear cells) fibrinoid degeneration of wall of blood vessels and granuloma (Klinge's rheumatoid knots), but the group of control hearts showed slight pathologica, changes. Next I verified serologically that mb freed in serum of chicken suffering from rice-illness, produces mb-autoantibodies by autoimmunization, and production of mb-autoantibodies is caused also in chicken serum of II group.

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I have already published that allergic myocarditis and allergic changes in the other organs is caused due to the sensitization with chickens mb in rice-illness, and mb of chicken suffering from rice-illness obtains autoantigenicity, producing thereby autoantibodies. Therefore, I assert that allergic myocarditis and myocardial damage due to mb was considered to make an important factor for the pathogenesis of beriberi heart.

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Changes of dye-density in blood after the injection of dye T-1824 were studied in rabbits which have, as stated in part I, experimental disturbance of hemodymanics in heart. It was shown that the time needed for the appearance of maximal dye density after dye-injection was prolonged in accordance with the development of hemodynamical disturbance of heart. This fact means not only the prolongation of mean circulation time but relative increase of the blood which take less part in blood circulation because of its too slow moving. The latter means the iner ease of relative depot of blood. The same conclusion was also obtained by the 2nd investigation i. e. the analysis of mixing grad ient of dye ((Δc)/(cΔt)) which the author proposed in this treaty to use in the investigation of the change of dye density in blood (C: dye density in blood, t: time)

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