1. Kidney angiotensinases are located in two kinds of subcellular fraction-lysosomal and microsomal. Lysosomal angiotensinase is active at an acid pH and inhibited by DFP, suggesting a relationship to plasma acid angiotensinase. Most of the activity was released from the particles by freezing and thawing. The microsomal enzyme is active near neutral pH, activated by calcium ion and inhibited by EDTA . 2. About 70 per cent of renin activity was released from the subcellular particles in lysosomal fraction of rat kidney by freeze-thaw method. It revealed only one peak on either Sephadex G-100 gel filtration or DEAE-cellulose column chromatography. The molecular weight of renin was calculated as 40, 000-50, 000. 3. At least three components of acid ATPase were found in lysosomal fraction of rat kidney by DEAE-cellulose column chromatography.

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The incidence and relative frequencies of congenital heart disease in school children were estimated by a field investigation. All the primary and the secondary school children in Otsu, a middle city of Japan, were investigated a few consecutive years for this study. In all 26, 177 children were examined, of whom 85 had congenital heart disease, giving an over-all rate of 3.2 per 1000. The most common malformation was ventricular septal defect, after which atrial septal defect and patent ductus arteriosus followed. An incidence of 3.2 per 1000 is intermediate among the previous results in these age group.

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The spatial magnitude, velocity and acceleration electrocardiograph, an analog computer specially designed for on line and real time analysis of spatial vectorcardiograms, were introduced and evaluated for clinical applications. Spatial magnitude, velocity and acceleration of vectorcardiographic loops were automatically recorded. Definite normal patterns were observed for these tracings and they changed in characteristic ways in various pathologic situations. Spatial velocity electrocardiograms could diagnose abnormal ventricular depolarization in cases whose standard electrocardiograms were not diagnostic. The importance of "abnormal velocity of spatial T loop" was stressed as a parameter of myocardial damage.

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Spontaneously hypertensive rats, renal hypertensive rats, DCA hypertensive rats, neurogenic hypertensive rats and control rats totalling 360 were killed under minimum stress. The noradrenaline in the adrenal medulla was stained by COUPLAND et al.'s glutaraldehyde osmium tetroxide method and the dimensional changes of noradrenaline storing cell islets were studied. In this experiment, spontaneously hypertensive rats were divided into four stages through their survival duration : until 30th day after birth, the 40th to 60th day after birth, the 5th to 7th month after birth and over one year after birth. Renal hypertensive rats, DCA hypertensive rats and neurogenic hypertensive rats were divided into four stages: the prehypertensive stage, the early stage of the 5th to the 24th day after operation, the middle stage of the 3rd month after operation and late stage of the 6th month after operation. Findings in spontaneously hypertensive rats, renal hypertensive rats, DCA hypertensive rats and neurogenic hypertensive rats were compared with those in control rats with almost the same survival duration. (1) The noradrenaline storing cell islets in the adrenal medulla became stainable from the 6th day after birth in both cases of spontaneously hypertensive rats and control rats. After that, the intensity of staining became stronger and after the 15th day, it maintained constant intensity. (2) The area of noradrenalune storing cell islets of the adrenal medulla in spontaneously hypertensive rats on the 6th day after birth was 9.6 per cent, about 1.2 times as large as that of control rats (8.1%) and after that as days passed, the area became larger. On the 10th day, that of spontaneously hypertensive rats was 14.1 per cent, about 1.5 times as large as that of control rats (9.1%), on the 18th day, 21.7 per cent, about 2 times as large as that of control rats (10.5%), and after that the state was constant until one year after birth, when it decreased a little. Spontaneously hypertensive rats develop hypertension in the 8th week after birth while the area of noradrenaline storing cell islets in the adrenal medulla becomes about 2 times as large as that of control rats before the development of hypertension, and this state remains constant after the development of hypertension. (3) As for the area of noradrenaline storing cell islets in the adrenal medulla of renal hypertensive rats, DCA hypertensive rats and neurogenic hypertensive rats, the following results were obtained : (a) In the prehypertensive stage, the areas in three kinds of hypertensive rats did not increase as in the case of spontaneously hypertensive rats, and there was no significant difference from that of control rats. (b) However, the area of noradrenaline storing cell islets in the adrenal medulla increased immediately after the development of hypertension. (i) Renal hypertensive rats showed an increase in the area; 17.8 per cent in the early stage, 17.9 per cent in the middle stage and 19.1 per cent in the late stage, and their values were 1.3 times, 1.5 times and 1.6 times as large as that of control rats. (ii) In the case of DCA hypertensive rats, the area was 19.9 per cent in the early stage, 20.5 per cent in the middle stage and 20.4 per cent in the late stage, showing an increase of 1.4 times, 1.6 times and 1.7 times in comparison with that of control rats. (iii) In the case of neurogenic hypertensive rats, the area was 21.4 per cent in the early stage, 23.5 per cent in the middle stage, 26.3 per cent in the late stage, and was 1.4 times, 1.7 times and 1.8 times as large as that of control rats, respectively, that is, in renal and DCA hypertensive rats, the grade of increase in the area was always smaller than that of spontaneously hypertensive rats but neurogenic hypertensive rats showed almost the same value as that of spontaneously hypertensive rats in the late stage. (c) The intensity of staining of noradrenaline storing cell islets did not show any difference fr

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The reaction of noradrenaline in the adrenal medulla was observed by COUPLAND et al.'s method under various experimental conditions such as rotating exercise, anesthesia, operation, disease and by using 175 spontaneously hypertensive rats and control rats and the following results were obtained. (1) Rotating exercise decreased the area of the noradrenaline storing cell islets both in spontaneously hypertensive rats and in control rats. Spontaneously hypertensive rats showed a higher rate of decrease and greater grade of decrease than control rats. As for the grade of decrease during the various duration of exercise, it was the highest within the first 30 seconds of exercise and after that, even though the duration of exercise was longer, only a slight decrease was observed. (2) When the rats rested after 1 minute of rotating exercise, the area of the noradrenaline storing cell islets in the adrenal medulla was restored gradually and after 1 hour of rest, the area of the noradrenaline storing cell islets of the adrenal medulla in spontaneously hypertensive rats was restored to the same state found before the exercise was loaded, but control rats showed only, 82 per cent restoration. (3) The area of the noradrenaline storing cell islets both in, spontaneously hypertensive rats and in control, rats remarkably decreased under Nembutal anesthesia and the grade of decrease in the former was greater but there was no difference in the rate of decrease between spontaneously hypertensive rats and control rats. (4) The area of the noradrenaline storing cell islets after the resuscitation from Nembutal anesthesia tended to decrease until the 12th hour after Nembutal injection and tended to increase after that, and 24 hours after Nembutal injection, the area of spontaneously hypertensive rats was restored to 77.5 per cent of that under the minimum stress and that of control rats was restored to 80.6 per cent. However, the actual grade of restoration was greater in the former than in the latter. (5) A decrease in the area of the noradrenaline storing cell islets at the time of operation under Nembutal anesthesia was more remarkable than simply under Nembutal anesthesia without operation. The grade of decrease and the rate of decrease in the area of noradrenaline storing cell islets in spontaneously hypertensive rats were greater than those of control rats. (6) The area of the noradrenaline storing cell islets of the adrenal medulla in spontaneously hypertensive rats decreased from 60 per cent to 0 per cent of the area under the minimum stress when they suffered from severe pneumonia. (7) As time elapsed after death, the intensity of the staining of the noradrenaline storing cell islets both in spontaneously hypertensive rats and in control rats decreased and the speed of the decrease in spontaneously hypertensive rats was quicker than that of control rats by 2 to 4 hours. The area of noradrenaline storing cell islets in spontaneously hypertensive rats and in control rats decreased gradually as time elapsed after death, and the rate of the decrease in the area was greater in spontaneously hypertensive rats than in control rats (8) From the above-mentioned results, it can be suggested that both synthesis and secretion of the noradrenaline of the adrenal medulla in spontaneously hypertensive rats are increased as compared with those of control rats.

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In the previous paper published from this department, it was reported that intramuscular reserpine administration to pulmonary and cardiac patients resulted in decrease of pulmonary artery pressure. It was found in addition, through the study at that time, that arterial oxygen saturation (SaO₂) also decreased in most of these cases. It was aimed, therefore, in this presentation to estimate the effects of reserpine upon ventilation, ventilation perfusion relationship in the lung, diffusing capacity of the lung and metabolic rate, for further analysis of the factors participating to the reserpine induced decrease in SaO₂. Materials and Methods In 15 patients with chronic pulmonary disease (6 with chronic pulmonary emphysema, 6 with bronchial asthma, 1 with bronchiectasis, 1 with pulmonary fibrosis, and 1 with chronic bronchitis) and 15 patients with chronic cardiac disease (3 with mitral stenosis, 3 with mitral insufficiency, 1 with mitral steno-insufficiency, 2 with aortic stenosis, 2 with atrial septal defect, and 4 with pulmonic stenosis), right heart catheterization was performed, then 1 to 2mg reserpine was injected intramuscularly. Respiratory functions and pulmonary circulations were studied before and 90 minutes after reserpine injection. Results Arterial oxygen saturation (SaO₂) decreased in 24 cases after reserpine administration. In patients with chronic pulmonary disease, 13 cases showed decrease in SaO₂ and the change was within a range of 4 to -13 (average -5.7) per cent. In patients with chronic cardiac disease, 11 showed decrease in SaO₂ and the change was within a range of 2 to -7 (average -2.1) per cent. In 4 cases with pulmonic stenosis the decrease in SaO₂ was only 0.8 per cent on an average. I. Changes in ventilatory functions, oxygen uptake and respiratory dead space and its relations to the changes in SaO₂.

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As an approach to investigate the manner with which the cardiovascular sounds and murmurs are transmitted, the intensity distribution of the sounds or murmurs on the surface of the chest wall was studied. The way of transmission of waves with the vibration of unitary frequencies to the surface of the chest wall was also studied through the examination of the intensity distribution of each vibration. Material and Methods The first and second heart sounds in 8 young normal men (19 to 25 years old), and the systolic murmurs in 7 patients with small. ventricular septal defect (19 to 33 years old) were studied. The apparatus for this study consisted of a moving coil direct-contact microphone, a pre-amplifier, a band pass filter with self-contained AC amplifier, an attenuator, a cathode-ray ocilloscope and a long-recording camera. In 6 normal men (19 to 24 years old), the way of transmission of the vibrations to the surface of their chest wall was studied. For this purpose, an oscillator, a frequency counter, a voltmeter, a vibrator, a moving coil direct-contact microphone, a band pass filter and a level recorder were used. Results The frequency intensity spectra of the first and second heart sounds at the points of maximum intensity on the chest wall were examined in one of the normal subjects. The same characteristics were investigated in one of the patients with ventricular septal defect at the point of maximum intensity of the murmur. The higher the cycle of their component frequency among the spectra of the normal heart sounds was, the lower the intensities of the first and second heart sounds became, that is, the intensities decreased at a rate of 15 decibels per octave for the frequency range of 50 to 1008 cycle per second. The same relation was observed between the frequency and the intensity in the spectrum of the murmur of V.S.D. (Roger's murur), that is, the intensity decreased at a rate of 6dB/ octave for the frequency range of 50 to 504cps and at a rate of 18dB/octave for 504 to 1008 cps.

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