Investigation was performed on the relation between the electrocardiographic findings in the cardiac patient of any etiology and pathologic findings of the specially made specimen of the heart after their death and to infer the relation between electrocardiographic pattern and the functional state of the heart muscle. Edematous degeneration of the heart muscle and the epicardium yielded in epicardial electrocardiogram ST elevation, and necrosis of the heart muscle Q wave. Prominent notching of QRS wave in such leads as I, II, V₅ and V₆ indicated diffuse myocardial changes in the heart. In the case showing depressed ST segment and lowered or inverted T wave, there were found scattered fibrosis and edematous degeneration of the myocardium in the subendocardial layers of the left ventricle. In the case with hypertrophic pattern of electrocardiogram also showed the same changes.

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The results of oral chloroquine treatment of 13 cases of nephritis were described and the beneficial effects were obtained in nearly all cases. The mechanism of chloroquine effect was discussed from the fluoro-microscopic findings of kidneys and the results of experimental studies on the anti-inflammatory effect of the related compounds.

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It has been said that nor-adrenalin exerts a vaso-dilator action on coronary vessels. There are a few investigators, however, who claim a vaso-constrictor action of the drug on coronary vessels. The author, as in part II, examined the action of nor-adrenalin on the coronary circulation following a direct infusion of the drug into the left coronary artery by the coronary catheterization in anesthetized, closed-chest dogs. Electrocardiographic changes caused by the infusion of nor-adrenalin were also studied. Method In addition to the experimental method described in part I, the left coronary was also perfused from a donor dog's femoral artery at a constant blood pressure. The experiments were performed 11 times on 5 adult dogs. Leads C_ψD and C_ψS were mostly used in taking electrocardiograms. Results (1) Experiments with coronary artery perfusion from the dog's own femoral artery (a) With 0.013 mg. of nor-adrenalin coronary blood flow increased. Both coronary wedge pressure and femoral arterial pressure also showed a rise. (b) Infusion of 0.13mg. of nor-adrenalin caused an increase in coronary blood flow, and a rise both in the coronary wedge pressure and the femoral arterial pressure. (c) With 0.33mg. of nor-adrenalin coronary blood flow markedly increased. Both coronary wedge pressure and femoral arterial pressure were elevated. (d) When 0.13mg. of nor-adrenalin were infused after the atropinization, coronary blood flow increased, and both coronary wedge pressure and femoral arterial pressure rose markedly. Single use of atropine caused changes neither in the coronary blood flow nor in the blood pressure. (2) Experiments with coronary artery perfusion from a donor dog's femoral artery under constant blood pressure. (a) With 0.013mg. of nor-adrenalin coronary blood flow decreased, while coronary wedge pressure and femoral arterial pressure showed an elevation. (b) With 0.13mg. of nor-adrenalin coronary blood flow decreased, while coronary wedge pressure and femoral arterial pressure became elevated. (c) With 0.33mg. of nor-adrenalin coronary blood flow decreased, while coronary wedge pressure and femoral arterial pressure became markedly elevated. (d) When 0.13mg. of nor-adrenalin were infused after the atropinization, coronary blood flow decreased, and coronary wedge pressure and femoral arterial pressure became markedly elevated. Conclusions (1) Nor-adrenalin exerts a vaso-constrictor action on the coronary artery as adrenalin does. (2) Action of nor-adrenalin on the coronary vessels were strengthened with a previous administration of atropine. (3) The electrocardiogram showed a decrease in pulse rate, an elevation of the T wave, occasional occurrence of right bundle branch block or WPW syndrome. With a previous administration of atropine the electrocardiogram presented changes similar to those in the case of adrenalin infusion.

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As factors controlling the venous pressure one can reckon the heart function, the tonicity of the venous wall, the amount of blood in circulation, respiration, the force of gravity and others. Whereas viewing solely from the stand point of the heart function, the venous pressure may be interpreted as representation of the balance between the efferent pressure of the left ventricle through the venous capillary system and the suction power of the right ventricle though the latter is not so marked. We have previously reported that physiologically there is a falling tendency in the venous pressure along with the advance of age despite a rising tendency in the arterial blood pressure. We have then deduced that a cause for this fact lies in the resistance to the blood flow due to the physiological sclerosis of arterioles. On the assumption that the resistance to the blood flow in the capillary system including arterioles may be ascertained if the arterial blood pressure and the cubital venous pressure are compared after eliminating the influence of the right ventricle by throwing various pressures on the upper arm, I have carried out such measurements and obtained some interesting results.Method The arterial blood pressure is measured after having the subject lie down in the recumbent position for 10 minutes. Next, with the use of a water level (the type designed by ourselves) and following Moritz and Tabora's technique, the puncture point is adjusted at 5 cm below the joint where the fourth rib is attached to the sternum. At this moment the elbow is slightly extended and is kept approximately at 45 degree angle with the axis of the body and the elbow is supported by either a pillow or folded towel. As a rule the puncture is made on V. med. cubiti but sometimes V. cephalica or V. basilica is selected depending upon the size and the direction of the vein. Using a spinal fluid puncturer, the glass-tube for measuring the blood pressure is filled with citrate to the height of about 10cm and a syringe is connected to the mandrin inlet and about 2cc citrate is kept in the mandrin. When the vein is punctured, the three-way stopcock is so turned as to connect the glass-tube with the puncture needle, and the lowest level of the fluid is taken as the venous pressure. Then, keeping the needle in the vein, a cuff is wounded around the upper arm and, at first, the pressure of 80 mmHg (at discretion) is thrown in. Thus the level of the fluid in the glass-tube rises and is stabilized. This level of the fluid is the venous pressure at the time when the pressure of 80 mmHg is thrown on the upper arm. It is necessary to avoid the blood from coagulation by injecting small amount of citrate from time to time by adjusting small amount of citrate from time to time by adjusting the three way stopcock. Next, when the pressure above the maximum blood pressure is thrown in the cuff and then it is gradually lowered, the elevated level of the fluid will fall. However. when the pressure reaches a certain point, the column of the fluid stops falling and begins to rise rapidly. When this pressure is sustained for a little while, the level rises and becomes stabilized. This level is the maximum venous pressure, and the pressure thrown in the cuff is the strain pressure at that moment. Result Nine young persons selected were all female except one, and 11 elder persons were all male. The average age of the former was 22.9 years while that of the latter 54.6 years. The specific gravity of blood is 1050-1060, but in computing mmH₂O into mmHg, the specific gravity of mmH₂O is set at 1, 000. Moreover, the surface tension effect of the glass-tube was not eliminated. 1. The average arterial blood pressure of young persons is 119-63 mmHg and that of the venous pressure 101 mmH₂O. The average arterial pressure of elder persons is 130-81 mmHg and the venous pressure 60 mmH₂O. [the rest omitted]

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It has been known that the pulmonary edema is frequently accompanied by central nervous disorders. This state frequently found in autopsy. It has been assumed that the condition was due to an increased permeability of the pulmonary capillary caused by the disturbed innervation of cardiovascular region. The author has attempted to clarify the mechanism of the pulmonary edema by experimentally inducing preoptic lesions.Method A central nervous lesion was produced by the electric coagulation in rabbits and dogs, whose brains were fixed and lesions were identified later by the microscopic study. Lung tissues were microscopically observed and findings were classified by Jordan's Table ; the pulmonary edema was also evaluated in ways previously reported by this author. Lung body ratio was calculated by the weight of lung and that of body. Systemic blood pressure was measured directly from the femoral artery through the canula connected with a mercury manometer. Wedge pressure was measured optically by the venous catheterization. Cardiac output was estimated by the dyedilution method. Spinal cord was cut surgically at the level of Cerval cord I-III, and bilateral vagal nerves at the cevical level, both under the artificial respiration. Results I. Pulmonary findings and systemic blood pressure in diencephalic lesions in rabbits. 1) Group of preoptic lesion Animals showed excitement after operation, and systemic blood pressure was elevated at first abruptly and fell gradually after a few minutes resulting in death. The existence of pulmonary edema was definitely proved both macroscopically and microscopically : there was an intra-alveolar edema accompanied by capillary congestion. Lung body ratio was high as compared with the normal. Pulmonary edema was found in 15 (75%) of 20 cases, but no correlation could be obtained between the grade of the pulmonary edema and the extent of preoptic lesion. 2) Group of hypothalamic lesion Systemic blood pressure has shown only slight fluctuation and neither macroscopically nor microscopically were any pathologic finding obtainable. Lung body ratio was also within normal ranges. In this group, pulmonary edema was found in only one (7%) of 15 cases. II. Role of the spinal nervous system and vagal nerves in pulmonary edema induced by the preoptic lesion. 1) Group of spinal transection As cervical spinal transection has been followed by a sudden fall of the blood pressure, a preoptic lesion was produced after the change of blood pressure was recovered by the transfusion of dextran or P.V.P. No pathological findings occurred in lungs and systemic blood pressure this group. 2) Group of the vagotomy Systemic blood pressure fell transiently, and recovered rather quickly. When a preoptic lesion was produced thereafter, blood pressure was abruptly elevated and began to fall in a few minutes ; most of the animals died. The lungs have shown the same degree of pulmonory edema as in the group of the preoptic lesion. III. Hemodynamic changes caused by preoptic or hypothalamic lesions in dogs. 1) Group of preoptic lesions. Pulmonary edema was found in 75% of this group. Elevation of systemic blood pressure (40±15 mmHg), elevation of wedge pressure (41±13 mmHg) and decrease of cardiac output (26±6%) were observed in these cases. 2) Group of hypothalamic lesions. The lungs showed no pathological findings, and elevation of systemic (12±5 mmHg) and wedge pressure (7±3 mmHg), and decrease of cardiac output (12±6%) were not so severe in degree as compared with the group of the preoptic lesion. Discussion Although anatomically the preoptic area belongs to the telencephalon, functionally not only this area but also the hypothalamus are closely associated with the autonomic nervous center. But it has not been proved whether it behaves the sympathetically or parasympathetically. [the rest omitted]

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It has been said that anisocoria had been rarely observed in cardiac disease, although it had been frequently found in pulmonary disease. Anisocoria associated with angina pectoris is expected to be one of the important objective findings which represent the irritation of afferent cardiac nerve. Seven cases of cardiac patients associated with anisocoria are described in this paper. Case Number 1 was a 32 year old man diagnosed as combined valvular disease caused by the acute rheumatic fever. Two years before admission he complained of anginal pain or precordial discomfort frequently. At the time of admission he was in the state of congestive heart failure. But neither anginal attack nor anisocoria was observed. Serum examination of syphilis was negative. After the administration of digitalis and diuretics the sign of congestive heart failure improved. Thirtyfive days after the admission he complained of severe anginal pain, which radiated to the left shoulder. Precordial discomfort continued for the following two days. About 12 hours after the attack anisocoria was perceived. Besides the dilation of the left pupil, no other abnormal neurological findings were observed. Three days later anisocoria disappeared. This careful observation demonstrated a certain relationship between anginal pain and anisocoria. Dilation of the left pupil seemed to be resulted from the stimulation of the left cervical sympathetic fibers which might be irritated reflexly by the impulse from the afferent cardiac nerve. Anisocoria was also observed in case of acute attacks or anginal stages of other six cases who had myocardial infarction.

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