Re-evaluation of Q-1 and 2-OS intervals and (Q-1)-(2-OS) index was attempted on preoperative phonocardiogram in mitral stenosis. Fibrosis of mitral value relates to Q-1 interval and this disturbs the correlation between Q-1 interval and the size of mitral orifice and left atrial pressure. 2-OS interval showed good correlation to the size of mitral orifice and left atrial pressure. The effect of fibrosis of mitral valve on this interval seems little. (Q-1)-(2-OS) index showed rough correlation to the size of mitral orifice but less correlation to left atrial pressure, probably due to fibrosis of mitral valve. Postoperative phonocardiograms reveal the clinical course of patient postoperatively and preoperative value of Q-1 and 2-OS intervals return toward normal value unless congestive failure or incomplete commissurotomy present.

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The phonocardiograms of Fallot's tetralogy, pure pulmonary stenosis, ASD, VSD were analysed concerning systolic murmur, particulary Q-M.S.M./Q-IIa, the ratio of the time interval, Q-M.S.M. (from Q to the peak of systolic murmur) to the time interval, Q-IIa, (the duration of systole), and splitting of 2nd heart sound in term of anatomico-physiological relationships. 1) In the tetralogy of Fallot, the 4 classification types of systolic murmur gave the useful informations for the evaluation of the stenotic type, either valvular, infundibular or both. 2) In pure pulmonary stenosis the right ventricular pressure was able to be estimated on the basis of Q-M.S.M./Q-IIa and IIa-IIp interval. 3) In ASD Q-M.S.M./Q-IIa was determined by the functional pressure gradient across the pulmonary valve 4) In VSD Q-M.S.M./Q-IIa (calculated from the systolic murmur recorded over the left 3rd intercostal space) roughly represented degree of pulmonary hypertention.

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The elasticity of the vascular wall has been the subject of many studies either with surgical or without surgical methods. The present author attempted to measure the elasticity of the arterial wall from the pulse wave curve recordable at the brachial artery and with a set of rather bold assumptions. Namely, the author assumed the arterial wall as a simple physical system with elasticity. Under this assumption the following equation will apply to the movement of the arterial wall: md²x/dt²=-Kx x=Sin ωt ω=2π/T T=2π√(m/K) where m : unit mass of the arterial wall tissue x : distance of the dislocation of a fixed point on the arterial wall vertical to the axis of the artery k : coefficient of elasticity T : period of sine wave The measurement of T will then allow the estimation of K, the coefficient of elasticity. Since, on the other hand, the velocity of the pulse wave propagation is related to the elasticity coefficient as follows : V∝√(p/K) there is another method of estimating the elasticity coefficient of the arterial wall. Methods Materials used consisted of three groups, (a) normal group, (b) arteriosclerotic group and (c) non-arteriosclerotic group consisting of cases with juvenile hypertension, nephritis and cardiac disease. The pulse wave was measured from the brachial artery by such arrangements that each pulse wave caused a corresponding change in the electrical capacity of the system which was presented to a condense microphone. At the same time, occlusion was applied 20cm distal to the point of the pulse wave recording by tighteing a vinyl-covered rubber band around the arm in order to measure the period of the reflected wave component (will be accentuated by occlusion) and measure the occlusion. Following this, the injection of TEAB or noradrenalin was performed and Pulse waves were recorded before and after injection (in this case, too, with and without occlusion). Throughout the course of these tests, simultaneous electrocardiograms were recorded by the third limb lead. The duration of time intervening between the R wave of electrocardiogram and the origin of ascending limb of the pulse wave gave the pulse wave arrival time. In this way the percentage change in pulse ware arrival time due to occlusion was also determined.

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The causal relations between various neuroses and the distribution of subclinical adhesive arachnoiditis cerebrospinalis have been extensively studied by Maekawa and his students. The neurocirculatory asthenia (N.C.A.), a type of neurosis, is frequently associated with abnormal electrocardiograms. It is also known that the stimulation of the peripheral sympathetic nerve produces electrocardiograms of "coronary insufficiency" pattern. In this paper the author tried to elucidate the possible role of the spinal sympathetic nervous system supplying the heart in the pathogenesis of N.C.A. by studying the effect of the electrical stimulation of the spinal cord in dogs on the electrocardiograms. Methods After adult dogs were laminectomized under anesthesia, a pair of concentric electrodes was inserted into the spinal cord, and the electrical stimulation was applied at 4 to 15 volts for about 5 to 15 seconds. Electrocardiograms were recorded before, during and after the electrical stimulation. Results and Discussion In 30 of 36 tested animals the electrical stimulation of the spinal cord produced electrocardiographic changes in ST and T waves. Although changes could be produced either with the upper thoracic cord or lower thoracic cord stimulation, electrocardiographic changes were more frequent in incidence and severe in degree with the former mode of the stimulation than with the latter. A still stronger effect could be produced when the two areas were stimulated simultaneously. The maximum effect was obtained at 2.5 mm depth of the insertion of the stimulating electrode; in this case the tip of the electrode was located near the lateral horn of the spinal cord. Although the electrical stimulation of the spinal cord produced an elevation of the blood pressure concomitantly with the electrocardiographic changes, the observed electrocardiographic changes were not possibly reactions secondary to the elevation of the blood pressure. Altered electrocardiograms and elevated blood pressure are probably two distinct manifestations of a single reaction process of the organism to the stimulation, i.e., the coronary vasoconstriction on the one hand, and generallized peripheral vasoconstriction on the other.

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Among the various methods proposed for the treatment of acute pulmonary edema, there has been known no definitive method to inhibit permeability of the pulmonary capillaries. On the basis of abilities of adrenocorticoids- to inhibit capillary permeability and to reduce capillary fragility, the author conducted a series of clinical investigations and proved their efficacy. Hydrocortisone was tested for its therapeutic value in experimental pulmonary edema of different pathophysiology produced by three different techniques. A) Materials and Methods 1) Nerogenic pulmonary edema by Reilly phenomenon. (Stimulation of cervical sympathetics in rabbits.) 2) ANTU pulmonary edema in rats. 3) Post-operative acute pulmonary edema produced by the sequence of pneumonectomy, anoxia then intravenous infusion in dogs. B) Methods of administering hydrocortisone. In groups 1 and 2, hydrocortisone 3 mgm per kilogram of body weight was given prophylactically one hour prior to the start of the procedure to produce pulmonary edema. In group 3, hydrocortisone 3 mgm per kilogram of body weight was given by intravenous infusion together with IPPB/i O₂ at the establishment of pulmonary edema. A group of dogs was treated with IPPB/i O₂ alone as a control. C) Evaluation of therapeutic efficacy. Therapeutic efficacy was compared among the groups mainly on the basis of pathological findings, macroscopically, histologically and by water content of the lungs, upon sacrificing. In addition. prolonged survival time was taken into account in group 2. In group 3, such parameters as respiratory and circulatory functions (pulse rate, femoral arterial pressure, central venous pressure, pulmonary arterial pressure, pulmonary capillary pressure, oxygen saturation and microscopic observation of the omental capillary vessels) as well as X-ray findings of the chest were also considered. Result and Conclusion 1) Excessive stimulation of the cervical sympathetic nerves caused marked congestion in the pulmonary capillaries, hemorrhage and edema into alveoli in rabbits. Hydrocortisone given prophylactically in a dose of 3 mgm. per kilogram of body weight prevented these changes almost completely. 2) The lung of rats given ANTU appeared like liver in consistency, with intense hemorrhage and edema, and all the animals died within four hours. Hydrocortisone given prophylactically in a dose of 3 mgm per kilogram of body weight suppressed those changes and prolonged the survival period to 16 hours or more. 3) Many of the dogs subjected to the sequence of pneumonectomy, anoxia and intravenous infusion developed in typical pulmonary edema. Although improvements in respiratory and circulatory dynamics were noted in the group treated solely with IPPB/i O₂, improvements in oxygen saturation, and blood flow in omental capillaries were better in the group treated with hydrocortisone in addition to IPPB/i O₂. This was reflected in pathohistological findings and JORDAN II-IV changes still persisted in the control group (IPPB only) whereas in the group treated with hydrocortisone and IPPB only JORDAN C-II changes were noted, and water content of lungs returned to the value noted before edema developed.

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The congestive heart failure occasionally occurs in the patients with chronic pulmonary hypertension stewed from chronic pulmonary diseases. Since this type of the heart failure in generally incurable, it is clinically important to detect the cardiocirculatory disturbances in these cases before the clinical symptoms of the heart failure develop. Then, the cardiopulmonary functions, especially the circulatory dynamics, in chronic pulmonary hypertensive patients were examined in this study. Material and Method The patients employed in this study were 32 cases of chronic pulmonary diseases, consisting of 15 cases of chroinc pulmonary emphysema, 1 of emphysematous bullae, 6 of bronchiectasis, 1 of pulmonary fibrosis and 9 of pulmonary tuberculosis complicated with either extensive pleural scar, chronic pulmonary emphysema or bronchiectasis, or after the chest surgery. All the cases had pulmonary hypertension, which was proved by means of cardiac catheterization. The data in 25 cases of chronic pulmonary diseases and of normal pulmonary arterial pressure were used as control. The analysis of expired gas and blood gas was done with a Scholander gas analyzer and Van Slyke-Neill apparatus, respectively. The pH of blood was determined using a Cambridge pH meter with a glass electrode. The pressures in the central veins, right heart and pulmonary circuit were recorded through Stat ham P-23Db strain gauge manometer on Yokokawa photographic recorder, employing the level of the external jugular vein as a zero point. The cardiac output was determined by the direct Fick method. The circulating plasma volume and mean pulmonary circulation time (abbr. MCT) from main pulmonary artery or right ventricle to brachial artery were measured using Evans Blue (T-1824). The ratio of right ventricular residual volume to right ventricular end diastolic volume (abbr. RV/EDV) was determined by Ohashi method, a modification of Bing-Holt method. The total pulmonary vascular resistance was calculated by Aperia's formula.

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Concerning the metabolism of proteins in hypoxemia, in 1920, Graubitz, Tscherkes and Melnikova found increases in the total nitrogen and NH₃ of the urine when carbonmonoxide hypoxemia was induced in animals, which indicated an increase in protein breakdown. However, no report has appeared in the literature on the changes in human serum proteins under acute induced hypoxemia. Therefore, the author subjected normal individuals and patients with various diseases to low oxygen respiration with the intention of studying its influence on the serum proteins. Methods and Subjects Human subjects in a resting and fasting state were made to inhale a 10% oxygen gas mixture for 15 minutes. Blood samples were obtained from. the femoral artery before and at the end of the inhalation. Also, in some cases, blood of the hepatic vein was obtained by the hepatic catheterization method. Serum protein fractionation of these samples was done by paper electrophoresis. The results obtained were analysed and their relations to the data of blood gas and carbohydrate metabolites obtained by coworkers, were studied. A total of 27 subjects were studied, which included healthy individuals (16 cases) and patients with mild or moderate pulmonary tuberculosis, hypertension and arteriosclerosis. Hepatic catheterization was per-formed on 14 cases which included healthy individuals (10 cases) and patients with pulmonary tuberculosis, gastric ulcer or mild cholecystopathy. Low oxygen administration was done simultaneously on 6 of these cases. RESULTS I. SYSTEMIC ARTERIAL BLOOD 1) Changes in the serum protein fractions : The low oxygen inhalation caused a significant decrease of the albumin fraction and a significant increase of the aα₁ globulin fraction. All globulin fractions showed negative correlations with the albumin fraction before the low oxygen inhalation and the correlations were also seen after the inhalation in all fractions except the α₁ globulin fraction. In general, the albumin fraction was most easily affected by the hypoxemia and the major change of serum proteins caused by the low oxygen respiration was the decrease in the albumin.

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