From the pulmonary edema experimentally induced with epinephrine, authors have stated that increased venous return and reduced cardiac output, the latter is due to a suppressed cardiac function, are largely responsible for production of the pulmonary edema. The pressor action of epinephrine would be considered as one of the determinant factors. If so, epinephrine would be replaced with angiotensin for producing pulmonary edema. This is not a case, however, because of absence of an accelerating influence on the venous blood flow in angiotensin, in spite of the fact that epinephrine has a potent effect on the venous system through the autonomic nervous system. When these pressor substances are given to the animals subjected to the total ablation of baroreceptor nerves, the state of affairs is quite reverse; it is rather difficult to produce the pulmonary edema with epinephrine, but readily with angiotersin. This has suggested significance of the autonomic nervous system on the regulation of the venous return.

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In order to investigate the mechanism that high SGO-T level caused by acute myocardial infarction return to the normal level, the influence of the co-enzyme, pyridoxal phosphate (PAL-P), on SGO-T activity was studied. The changes of SGO-T activity with the addition of PAL-P in the cases with elevated SGO-T level produced experimentally was entirely different from that in the normal. In all of the former cases, a marked increase of SGO-T activity with the addition of PAL-P was recognized. In two clinical cases of acute posterior infarction, an increase of SGO-T activity to abnormal level was observed when PAL-P was added to the serum samples taken in the early stage of myocardial infarction. Therefore, measurement of the increase of SGO-T activity by adding PAL-P was considered to be useful for unveiling minimal discharge of GO-T into the blood.

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I have already pointed out that, in order to anticipate the cerebral vascular accident, the following are of most clinical importance.¹⁾ The one is the quantitative and qualitative analysis of cerebral arteriosclerosis and hypertension, the other is the investigation of circulatory regulation. Among them, the detection of cerebral arteriosclerosis is more valuable and difficult. Although this problem have been investigated by using many operative and non-operative method, the ideal technique for clinical use has not yet been developed. On the other hand, SATOMURA and KANEKO has initiated the unique technique of measuring cerebral circulation i e ultrasonic Doppler technique.²⁴⁾ In this study, several problems regarding to theoretical concept of the method are investigated.

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On the pathogenesis of myocardial infarction, there have been many works particularly with reference to coronary sclerosis, blood coagulation and stress. In recent years patients with myocardial infarction have been treated with anticoagulant. The subject of this treatment is to prevent the attacks of myocardial infarction by reducing blood coagulability with anticoagulant. However, the therapeutic and preventive effect of this treatment is not yet exactly established. In this paper it will be presented the results of experimental studies performed with reference to the role of blood coagulation and the effect of anticoagulant therapy in the prevention of infarction. Methods and Materials. In the experiments, rabbits were used, coronary sclerosis and myocardial infarction were produced by the injection of allylamine and homologous rabbit serum. Twenty female rabbits, weighed 2 to 3 kg., were divided into 4 groups A, B, C and D. Group A was given intravenously 15 mg/kg of allylamine 20 times and then 30 mg/kg 10 times every other day. Group B was given 2 ml of rabbit serum intravenously every other day after the treatment of allylamine as group A. Group C was given Warfarin orally after the treatment as group A and then injected rabbit serum as group B. During these procedure prothrombin was maintained as to keep the level of 10 to 25 per cent of normal. Group D was injected rabbit serum only. In each group, blood clotting factors were estimated and they were examined occasionally by electrocardiography. All servived rabbits were killed on about 100 days from the first injection of rabbit serum and investigated histologically. Prothrombin was estimated by Quick's one stage method. Factor V was determined by Wolf's method modified by MATSUOKA. Factor VII was estimated by Koller's method. Thromboplastin generation test was performed as described by BIGGS and DOUGLAS. Fibrinogen was estimated by tyrosine method. Whole blood clotting time was estimated by the method of LEE-WHITE.

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Thirty five year old man was admitted to Kobe Medical College Hospital on March 6th, 1961, because of the abnormally clear lung field of the left lobe shown in chest x-ray film. The patient presented no complaints. The family and past history contributory to the morbid state of the lung were negative. His respiration was costabdominal type, 16 per minute. No cardiac murmur was heard nor accentuation of the second pulmonary sound. The respiratory sounds were vesicular, , but scarcely audible in the left field of the lung. As referred, chest x-ray film was extremely, clear in the left lung field with just a few faint shadows in the upper lung field but the left hilar shadow was scarcely visible. The brbnchography revealed cytic dilatation in several bronchi in the left lower field. The pulmonary function test disclosed the normal vital capacity with obstructive impairment, including a slight increase in residual volume and slight reduction in the total lung capacity. Reduction in oxygen uptake in left lung lobe was most noticeable. It is due possibly to the reduced blood flow of the left pulmonary artery. The right heart catheterization failed to reveal any abnormal pulmonary circulation, the catheter however. could not pass through the left pulmonary artery due to its narrowing which was demonstrated by the angiocardiography. Narrowing of the pulmonary artery was found just distal to the bifurcation of the stem of the main pulmonary artery and the peripheral pulmonary arteries distal to the narrowing appeared slender, indicating an unilateral malformation of the pulmonary artery system.

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