Comparison of angiocardiographic and postmortem measurements of the ventricular wall thickness in dogs was made. Angiocardiographic thickness of the ventricular wall was found to be 7.4% thinner than that proved at autopsy. The notable merits and little demerits of angiocardiographic determination of ventricular hypertrophy as compared with postmortem measurement were briefly discussed. Various electrocardiographic criteria for LVH appeared to give relatively high positivity but they also showed a high incidence of false positives. New sets of the criteria for LVH are herein proposed to give better results. Only one half of cases with angiocardiographically confirmed RVH was diagnosed with existing criteria for RVH, and the diagnosis of CVH was found to be extremely inaccurate.

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An attempt was made to establish diagnostic programs for computer diagnosis of the electrocardiogram with FRANK'S lead system. The diagnostic logical trees employed the spatial parameters were contrived following the physician's diagnostic process on P-PQ, QRS and ST-T complex. Computer diagnoses were firstly made on the above three complexes individually, then conclusive diagnoses were made by another combination logics. A comparative review was made between computed and visually determined diagnoses on 205 subjects with various ECG findings. The present programs for computer diagnosis, apparently simple as they were, were inclusive of characteristics of the spatial vectorcardiogram, enabling the computer to successfully diagnose 205 records.

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1. Extensive lesions in medial anteromedian hypothalamus induced severe to moderate hypertension in Wistar rats. 2. Sites of lesions indispensable to the production of hypertension proved to be anterior hypothalamic area, ventromedial nucleus, anteromedian part of arcuate nucleus and periventricular nucleus located medial to these nuclei, while the lesions involving pituitary stalk, posterior portion of arcuate nucleus and large portions of mammillary region prevented the development. 3. This hypertension was potentiated by, or in some instances, dependent on salt loading. 4. In the hypertensive animals, remark-able adrenal hypertrophy was present in association with increased plasma corticosterone. Increase in plasma corticosterone was also detected in the hypothalamus-lesioned animals in the early hypertensive stage. 5. Adrenal glomerular zone was atrophied in many rats, subjected to medial anteromedian hypothalamic destructions. 6. Renal lesions, such as thickened capsules and basement membranes of proximal convolutions, often resulting in tubular deteriorations and cystic dilations, were observed in the animals with medial anteromedian hypothalamic lesions, regardless of whether they were hypertensive or not. 7. Vascular lesions detected in the rats which developed hypertension following hypothalamic lesions, were periarteritis nodosa, arteriolar necrosis, productive arteriolitis with or without fibrinoid necrosis and glomerular necrosis. 8. It is concluded that the augmented adrenocortical secretion, probably in conse-quence of eliminated corticoids feed-back mechanism due to hypothalamic lesions, plays the major role in the pathogenesis of this hypertension.

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It is no doubt that the edema is a state of abnormal retention and distribution of sodium and water and antidiuretic hormone (ADH) is the potent water conservatory hormone. A clinical and experimental study was made on the role of ADH in the causation of edema occurring in congestive heart failure. The correlations between ADH secretion and clinical findings were investigated and in addition, ADH secretion was estimated in dog with ascites. The result obtained showed that ADH secretion was increased in edematous state and ADH played a part in water reabsorption.

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Pressor and non-pressor aqueous extracts were separated from normal and ischemic rabbit kidney cortex by column chromatography and injected into test animals. Five to 6 test animals injected with the non-pressor extract from ischemic kidney developed vascular injuries especially in small cerebral arteries. This finding suggests that a non-pressor substance capable of producing vascular injury independent of renin is present in ischemic kidney cortex.

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Through the consecutive annual physical examination of four years' duration on the school children of the city of Otsu, we selected out 653 healthy children without evidence of heart disease, classified their electrocardiograms according to age, sex, heart position of WILSON and position of transitional zone, and measured amplitudes and durations of each deflection of these electrocardiograms. The criteria of the absence of heart disease were those of ZIEGLER. Thus maximum, minimum, mean, standard deviation and percentile distributions (upper: 97.5 percentile, lower: 2.5 percentile) were calculated and their normal values were decided. Percentile distributions were calculated according to the formula A of the appendix in SIMONSON'S monograph. This study consisted of 307 children of 13 years of age and 346 of 14 years of age. By means of these procedures the following results were obtained. 1 . Vertical and semi-vertical heart position of WILSON were predominant (93.1%) and transitional zone to the right of lead V₄ (CR-and CM position), namely counterclockwise rotation around the longitudinal axis of the heart were quite frequently observed (88.0%). (In this paper we classify these two positions (vertical and semi-vertical) into one oosition and call this position 'vertical heart position'). Consequently vertical heart position and counterclockwise rotation around the long axis of the heart were almost constantly observed in these age groups. 2. In respect to the amplitudes of the R and S waves, the heights and/or depths were greater in the male children than in the female children in almost all the leads (p≤0.01). And also these values were greater in the 13 year-old girls than in the 14 year-old girls, perhaps due to the rapid development of sub-cutaneous fat tissues in these age groups (p≤ 0.01). 3. In the present study the mean values of the amplitudes of the R and S waves in the chest leads were greater than those of Koss-MANN, ZIEGLER, and SOKOLOW-LYON (p≤0.01). The upper limits (97.5 percentile) obtained by us were roughly identical with maximal normal values between 10 and 20 years of age proposed by KOSSMANN, but our results exhibited much greater values than those of maximal normals of SOKOLOW and FRIEDLANDER.

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A conception of "Dysproteinamische Myo-kardose" was first brought out by F. WUHR-MANN in 1950. After that, T. NANGU studied statistically the relation between electrocardiographic abnormalities and those of serum protein in various hepatic diseases, and made it clear. On the other hand, it is well known that generally speaking the variations of serum electrolytes are also important for the electrocardiographic changes, and many literatures concerning this problem have been listed. But the systematic study particularly pointed toward the relation between serum electrolytes and the electrocardiographic findings in hepatic diseases has scarcely been found. Therefore, the authors intended to make clear this problem, comparing influences of the dyselectrolytemia with those of the dysproteinemia upon electrocardiographic changes in hepatic diseases especially in hepatic cirrhosis. MATERIALS AND METHOD Twenty four cases of acute hepatitis, nine-teen cases of chronic hepatitis and fourty two cases of cirrhosis of the liver were included in the whole 85 materials without a history of the circulatory diseases. Measurements of the serum sodium and potassium were performed on the same day with the electrocardiography.

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Many studies on the cardiac transmembrane potentials and on the sequence of activation of the heart have been reported. However, there have been only a few reports on the transmembrane potentials of the musculature in the great vessels proximal to the heart and on the excitation conduction from the heart to these vessels. Previously, MASHIBA and coworkers reported that, in the in situ rabbit, the sinus node impulse spreads not only to the atrial muscle but also to the musculature in the vena cava. They called this phenomenon "sinocaval conduction". To extend this observation, in the present paper, the author studied on the sinocaval conduction of the rabbit atriocaval preparation with the microelectrode methods. METHODS In the rabbit, there are three venaec avae which empty into the right atrium by separate ostia: right superior vena cava, left superior vena cava and inferior vena eava. In all experiments, the preparation consisting of atria resected together with three venae cavae (atriocaval preparation) was used (Fig. 1). The preparation was perfused with oxygenated Tyrode solution at a constant temperature (35-37°C) and with a constant flow. As for intracellular electrode, the LING-GERARD type of microelectrode was used which was filled with 3 M KCl solution and had 20-40 Megohm electrical resistance. RESULTS 1 . Shape of the transmembrane action potentials of the musculature in the rabbit venae cavae (Fig. 2 and 3). On the basis of the shape of the observed action potentials, 4 functional regions could be described in the vena caval tissues: I) sinus node, II) sinocaval (SC) areas, 111) superior venae cavae and IV) inferior vena cava. The features of the action potentials in the sinus node are the marked diastolic slow depolarization, the slow rate of rise, the low amplitude and the absence of overshoot.

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The relationship of acid mucopolysaccharides (AMPS) to atherogenesis has been the subject of a number of reports mainly from the stand-point of histochemical investigation. Two theories prevail ; one assumes that the deposition of AMPS in vessel walls is the first stage leading to atheromatous changes, the other assumes it is only a secondary change caused by deposition of lipid in the vessel wall. Recently, biochemical findings for arterial AMPS have developed rapidly, and several reports have dealt with atherosclerosis. But, since the various kinds of AMPS are similar in character, their chemical analysis is complicated and an interpretation of the results is was determined. accompanied with considerable difficulty. On the other hand, the function of AMPS as a polyanion should be taken into account in the understanding of atherogenesis. In order to study the relationship between arterial AMPS and atherosclerosis, the author observed the behavior of sulphate in the aortic wall and the physicochemical binding capacity between the polyanion and plasma protein fractions. MATERIALS AND METHODS 1. After removing the adventitias and a part of the medias of the aortas of rabbits with experimental atherosclerosis, the aortas were treated with Sudan III stain. They were divided into three groups, "none", "slight" and "moderate and severe" according to the degree of atherosclerosis. The degree was determined by the stained appearance. The materials divided were then hydrolyzed with a solution of aqua regia and distilled water mixed with equivalent volume. The sulphate in the aortas was determined by the method of MURAKAMI et al.

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In order to study the role of sulphated AMPS in the development of atherosclerosis, the sulphate analyses of human aortas, coronary arteries and basilar arteries was made using the method described in the first report. Furthermore, the affinity of human aortic AMPS to plasma protein fractions was investigated utilizing the paperchromatography and the fluorescent antibody technique. MATERIALS AND METHODS 1. Human aortas, coronary arteries and basilar arteries were obtained from autopsies. After removing the adventitias and a part of the medias, the vessel walls were stained with Sudan III. They were divided into 4 groups, "none slight" "moderate" and "severe", according to the degree of the atherosclerosis. The degree was determined by the stained appearance. The materials divided were then subjects to sulphate analysis using the method described in the first report. 2. Using the unidimensional descending technique, the chromatography was carried out on No. 50 Toyo paper with the citrated 28% ethanol saline solution. The samples applied are as follows; 1. Fibriongen 40mg/ml. 2. Heparin solution 3mg/ml. 3. Mixture of Fibriongen and heparin. 4. Mixture of fibrinogen and sulphated alginic acid 1.5mg/ml. 5. Mixture of human serum and human aortic AMPS 3mg/ml. 6. Mixture of human plasma and human aortic AMPS. 7. Heparinized plasma of rabbit. With RINGER'S solution as a solvent instead of the 28% ethanol solution, the chromatography of the mixture of fibrinogen and these AMPS solutions were also carried out by the same method. 3. Anti-human β-lipoprotein rabbit serum coupled fluorescein isothiocyanate and anti-human fibrin rabbit serum coupled the same were employed. The section of the aortas were treated with the fluoresceint-coupled antisera. The materials studied were obtained from autopsies, and the samples selected were irregular, slight yellow in colour and minimally elevated.

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