In all myocardial changes, pertaining to cardiac valvular disease except inflammatory changes, influence given to myocarcial changes histologidally by mechanical circulatory disturbance, that is, valvular insufficiency, has been studied by the author. The author experimentally produced the maximal cardiac valvular insufficiency for survival in a dog. His survey over 6 months is as follows: 1. In aortic insufficiency and mitral insufficiency. changes are classified into the periods of (1) hyperemia and bleeding, (2) cellular infiltration, and (3) scar-formation. 2. These changes appear just in papillar muscles in left ventricle. 3. The extents of above mentioned pathological changes are found proportionate to that of valvular insufficiency.

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To get some fundamental informations concerning the electrocardiogram in myocardial infarction, I tried a vectorial observation in the experiments by injurying the myocardium from the epicardial surface on the heart of the tord by using the vectorpolyography with scarce strain. (1) Immediately after the injury the RS-T junction was not located on the zero point but deviated toward the direction resembling that of the outward normal line at the centre of the injured surface. (2) The QRS loop in injury traced the course before injury for a certain moment after the start and then began to be deformed, pulling itself more and more toward the displaced RS-T junction in injury. (3) It was difficult to explain the above mentioned experimental results from the negativity theory by Fahr et al. (4) Using the renovated membrane theory by Wilson and others, I expressed the equations which are able to bring together complicated processes for the appearance of the monophasic curves of many kinds, from the onset of the QRS group to the displaced RS-T junction. (5) Trying a model calculation by the above stated equations in vectorcardiography when the myocardium is injured, I indicated that the vector of the RS-T junction in injury should be directed toward the vector sum of the moment of the equivalent electrical double sheet at the surface which bounds the injured and the uninjured region. As it may be considered that this direction of the vector sum resembles nearly the direction of the outward normal line at the centre of the injured surface, consequently the results of my experiments may be explained by my consideration. On calculation, vectorpolyography has the least strain in this department, too. (6) It was proved mathematically that the deformation of QRS loop should occur early when the portion is injured where the arrival of the excitation wave is early when not injured, and that should occur late when the portion is injured where the arrival is late.

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The changes in T_I (especially positive TI) height of guinea pig in each experimental course were investigated. A. Exp. I (Head→Tail×10") T in all cases shows the enlargement during exposure to the acceleration (3.5, 6, 8g). (Enlarged type). The time indicating the maximum enlargement of T during exposure to the acceler and the time returning to the original T-height after the cessation of centrifugalization are almost the same as those of P in the same kind of experiment, (see the Report I). Generally the max. enlargement (%) is likely to be greater in accordance with the increase of the magnitude of g exposed. B. Exp. II (Tail→Head×10") The general type of change in T-height in the experiment (3.5, 6g) is the "Reduced type," and the times indicating the max. reduction of T and returning to the original T-height in the experimental course are nearly the same as those of P in the same kind of expenment. The max. reduction (%) seems to be smaller in 6g rather than 3.5g-expeiment. C. Exp. III (to L. & R. along the Transverse axis×10") The general type of change in T-height is the "Enlarged type," and it's change in the experiment (3.5, 6g) is the very same as that seen in Exp. I. The max. enlargement (%) is nearly equall in the same g-experiment, even though the acceler. is directed to either L. or R., and is likely smaller than that in the same kind of experiment in A.

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Rabbits were sensitized with the same antigen as shown in report-I, and reinjected with heated diphtheria toxin (80℃×20 minutes). Myocardial change remained slighter, but capillary damage and frish hemorrhage were obserued in papillary muscle. In another group, 200 A. U. autitoxin was injected after sensitization, so the effect of the reinjection was deiriased. Without heart-muscle-phospho-sphatide, these changes were not so clear.

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The blood pressure and pulse rate of 50 persons, who were wounded in their head in battle, varied with a conversion of their pose standard (converted into various positions: in lying on their back, in standing, in crouching, in crouching with their heads dawn, in standing again) and also a bodily and mental working-lord, in contrast of 20 persons in good health, 20 cases of the essential hypertension and 5 cases of perkinsonism. The head wounded patients, the essential hypetension and perkinsonism have more abnormal blood pressure control than the healthy condition, and these abnormal phenomena (in the conversion of pose standard and the mental working-load) were much improved by LUMINAL. These experiments indicated that the abnormal blood pressure control were centrical or nervous by origin. The fact that the perkinsonism, a brain stem disease, presented also the very same abnormal blood pressure control, can confirm that these abnormal phenomena are nothing but the centrical.

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