In order to evaluate the accuracy of the electrocardiographic criteria for the diagnosis of ventricular hypertrophy, end-diastolic angiocardiograms in left anterior oblique projection were performed in 152 patients from 18 to 65 years of age. The correlation between the ventricular wall thickness measured on 12×10 films and electrocardiographic findings were examined. Angiocardiographic analysis with regard to the ventricular wall thickness revealed 38 cases of LVH, 24 cases of RVH, 16 cases of CVH and 65 cases of normal thickness of both ventricular walls. The positivity and the false positivity by the criteria for LVH used were found to be 92.1 per cent and 53.8 per cent, respectively. "Rv₅₍₆₎+Sv₁≥35(40)mm" was more satisfactory than "Rv₅₍₆₎+Sv₁≥35mm" (68.4 per cent of positivity with 18.5 per cent of false positives for the former and 71.1 per cent of positivity with 35.4 per cent of false positives for the latter). High voltage in the extremity leads appeared to be of less value in the diagnosis of LVH. MORI's criteria, except "ΣLVP≥40(50)mm", had a lower incidence of false positives than SOKOLOW and LYON's voltage criteria on chest electrocardiogram. Pattern criteria of KIMURA gave the highest positivity when the presence of "one or more" of three conditions was accepted as satisfactory criteria for LVH, whereas it gave the lowest incidence of false positives with the fewest positive correlation when the presence of "two or more" of three conditions was applied. KATO's set of the criteria was found to be the most sensitive in the diagnosis of LVH, although each item itself was not so high diagnostic value. Finally it was concluded that the single criterion, whichever the voltage or the pattern criterion, was not satisfactory enough for the diagnosis of LVH, but the set of the two conditions appeared to be more useful. Herein proposed is the set of "Rv₅₍₆₎+Sv₁≥40(45)mm" (45mm is used for persons of 25 years old or younger) and the pattern of "S_III>s_II" as a diagnostic criteria for screening examination of LVH (90 per cent of positivity). And when the presence of "Rv₅₍₆₎+Sv₁>≥40(45)mm" with "S_III>S_II" or with "comparative ratio of R and S on chest leads over 10" was used as the criteria for LVH, it gave only 1.5 per cent of false positives with 50.0 per cent of positive correlation. This set of the criteria is useful to confirm the presence of LVH. The electrocardiographic diagnosis of RVH was made in 52.6 per cent by the criteria used in this study. The positive correlation was influenced by the ratio of the left ventricular wall thickness to that of the right. The positive correlation was found more frequently in RVH due to congenital heart disease than in RVH due to acquired heart disease. Among the various criteria for RVH, R/S ratio in V₁ over 1.0 and R/S in Lead I less than 1.0 may be concluded to be sensitive and RAD>110 degrees and RaVR≥5.0mm were found fairly to be specific. The significance of rSR' pattern in the right precordial leads with a normal QRS duration was briefly discussed. Poor reliability of electrocardiography was observed on the diagnosis of CVH (6.3 per cent of established diagnosis). It is notable fact that 8 of 16 patients who showed angiocardiographic evidence of CVH had hypertensive heart disease. The ratio of the left ventricular wall thickness to that of the right appeared to influence the incidence of positivity but no close relationship between them was obtained. MORI's criteria gave higher percentages in the positive correlation with CVH than that with LVH.

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Although atrial fibrillation and flutter have been studied for many years, the pathogenesis and the mechanism of these arrhythmias have not been established as yet. However, it is generally accepted that many factors might be responsible for the initiation of the arrhythmias; some of them have been proved in clinical and/or experimental studies. It is interesting that both atrial fibrillation and flutter can be obtained experimentally by various methods, because a method producing the atrial arrhythmias may suggest some of the contributing factors to initiate these arrhythmias. This study was attempted to produce atrial fibrillation experimentally by means of new methods. The author observed that atrial fibrillation could be obtained by vagal stimulation or epinephrine injection during vagal stimulation after intravenous infusion of the aqueous solution of sodium bicarbonate, and also of sodium lactate.

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The mechanisms of the development of the chronic cor pulmonale in various chronic pulmonary diseases are one of the interesting problems to be inquired, with its relation to the development of the pulmonary hypertension. In this study, the coronary sinus and the right cardiac catheterizations were performed simultaneously on chronic pulmonary diseases, and the coronary circulation was studied chiefly from the viewpoint of the oxygen metabolism, and pulmonary circulation hemodynamically. It was concluded from this investigation that hypoxia of the left ventricle existed in the chronic cor pulmonale, and that chronic hypoxemia due to the pulmonary insufficiency shows a different attitude from the acute-induced hypoxia in the coronary circulation.

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Selective breedings of male and female spontaneously hypertensive rats (OKAMOTO and AOKI) which showed persistent hypertension (blood pressure exceeding 150 mm.Hg) for over a month were repeated successively from F₅ rats in the same manner as mentioned in the previous report and rats from F₆ to F_&glt;12> have been obtained up to the present time. Chronological observations were performed on the body weight and blood pressure of a total of 740 spontaneously hypertensive rats, as well as of 60 control rats of the Wistar strain. Both body weight and blood pressure (by tail-water plethysmographic method) were measured once a week from 5 weeks of age through 60 weeks and the following results were obtained. 1. The body weight of the spontaneously hypertensive rats showed no significant difference as compared with that of the controls. 2. The blood pressure of the control rats was almost stationary after 10 weeks of age and never exceeded 140 mm.Hg throughout 60 weeks either in males or females. The increase in blood pressure of the spontaneously hypertensive rats showed no difference among the seven generations examined. The average systolic blood pressure of the spontaneously hypertensive rats rose with age and was significantly higher than that of the controls of the same ages after 10 weeks of age among all rats except the F₉ females, in which it was after 15 weeks. The levels of the average systolic blood pressure were about 190 mm.Hg in males and 180 mm.Hg in females at 30 weeks and after. 3. Some (6.7-10.0 per cent) of the control rats showed spontaneous hypertension with blood pressure levels not exceeding 160 mm. Hg after 15 weeks of age. In the spontaneously hypertensive rats development of spontaneous hypertension was observed even at 5 weeks of age and all animals had become hypertensive within 20 weeks. Severe hypertension with the blood pressure exceeding 200 mm.Hg began to be found at 10 weeks of age and its frequency averaged about 50 per cent in males and 30 per cent in females at 30 weeks of age. 4. The blood pressure of the male spontaneously hypertensive rats was about 12.2 mm.Hg above that of the females on the average. The males tended to develop into hypertension at a lower age than the females. 5. The coures of the blood pressure seemed to be fixed in the spontaneously hypertensive rats following F₆, and several stages were distinguished in relation to the blood pressure as follows. Namely, the period up to 6-7 weeks of age was referred to as the "prehypertensive stage", from 7 to 20 weeks as the "transitional stage of hypertension", from 20 to 25 weeks as the "initial stage of hypertension" and after 25 weeks as the "advanced stage of hypertension". 6. The spontaneous hypertension of rats seems to have characteristics similar to human essential hypertension in certain aspects, but identification of hypertension in the spontaneously hypertensive rats and human essential hypertension is a question for further study, and may be related to elucidation of the pathogenesis of essential hypertension.

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Spontaneously hypertensive rats (OKAMOTO and AOKI) were sacrificed in the pre-hypertensive stage (40 to 60 days after birth), initial stage (5 to 7 months after birth) or advanced stage of hypertension (13 to 17 months after birth). Twenty-one kinds of enzyme activity were examined histochemical in the adrenals, thyroid, kidneys, heart, liver and pancreas, and noradrenalin reaction was also applied to the adrenal medulla. Each positive finding in spontaneously hypertensive rats was obtained by comparing it with the reaction of the same sex normotensive Wistar strain rats with almost the same survival duration. 1) Glucose-6-phosphate dehydrogenase and triphosphopyridine nucleotide diaphorase activity increased in the zona fasciculata and reticularis of the adrenal cortex of spontaneously hypertensive rats with dominant elevation of the former activity in the middle and outer part of the fascicular zone from the pre-hypertensive stage. More prominent increase was observed after the incidence of hypertension. 2) The noradrenalin-storing cell islets in the adrenal medulla of spontaneously hypertensive rats indicated a stronger reaction with about twice the mean dimensional ratio to the whole adrenal medulla in all stages than was found in normotensives. 3) Acid phosphatase activity in the follicular cells of the thyroid in spontaneously hypertensive rats was elevated from the pre-hypertensive stage. 4) Adenosine triphosphatase activity of the renal interlobular arteries of spontaneously hypertensive rats showed an increase in about half the cases in the pre-hypertensive stage and in all cases after the incidence of hypertension. 5) Glucose-6-phosphate dehydrogenase and triphophopyridine nucleotide diaphorase activity in the zona glomerulosa of the adrenal cortex of spontaneously hypertensive rats rose after the incidence of hypertension, though the latter activity showed only a slightly in-creasing tendency. 6) Increase of adenosine triphosphatase activity in the walls of renal interlobular arteries and vasa afferens of spontaneously hypertensive rats was detected in all cases after the incidence of hypertension. 7) Gradual elevation of monoamine oxidase activity in the heart muscle of spontaneously hypertensive rats occurred after the incidence of hypertension. 8) No constant difference was found in the results of other kinds of enzyme histochemical comparisons of adrenals, thyroid, kidneys or heart, or in the enzyme histochemistry of the liver or pancreas, either. 9) From the above-mentioned evidence, it may be assumed that there exists from the pre-hypertensive stage in spontaneously hypertensive rats, an increase of (1) glucocorticoids synthesis in the adrenal cortex ; (2) either synthesis of noradrenalin, or retention of it in the adrenal medulla ; (3) secretory activity of the thyroid and (4) the contracting tendency of the renal vessels of medium caliber. In addition, after the incidence of hypertension, elevation of (5) aldosterone synthesis in the zona glomerulosa of the adrenal cortex ; (6) the contraction of the renal vessels and (7) the catecholamine metabolism, primarily the oxidative deamination in the heart muscle is also indicated.

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Histometrical studies were performed on the superior cervical sympathetic ganglia of the spontaneously hypertensive rats (OKAMOTO and AOKI) and the following results were obtained. 1. Weights of the ganglia of the spontaneously hypertensive rats were significantly heavier than those of the control normotensives in initial and advanced stages of hypertension. The difference in mean value corresponded to 45 per cent of weights of the controls in initial stage and 31 per cent in advanced stage. 2. Volumes of the ganglia, and nuclear and cellular size of the nerve cells involved in them were significantly larger in the spontaneously hypertensive rats than in the controls from pre-hypertensive stage to advanced stage of hypertension. The volume of the ganglion of the hypertensives exceeded that of the controls by 34, 23 and34 per cent in pre-hypertensive, initial and advanced stages, respectively. Those in nuclear size were 20, 19 and 29 per cent in respective stages, and cellular enlargement was in the range of 20-22 per cent throughout all stages. 3. Total numbers of the nerve cells in the ganglia revealed no significant difference among all materials examined. 4. Additional histopathological findings of the nerve cells showed moderate chromophilia and no meaningful degenerative changes in the spontaneously hypertensive rats as compared with the controls. The former was more remarkable in pre-hypertensive stage and initial stage of hypertension. 5. The probability of sympathetic hyperactivity in the spontaneously hypertensive rats was presumed from the above-mentioned results and discussed in relation to the recent studies in our laboratory.

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Reports on renal electrolyte metabolism at rest in healthy subjects and hypertension have been found since the initiation of renal clearance methods and renal vein catheterization. However, little results are available on the effect of low oxygen gas inhalation on it. The effects of low oxygen gas inhalation on visceral circulation-metabolism in several main organs have been studied at our department. The author attempted to examine its effect on renal electrolyte (Na and K) metabolism. Methods and Subjects Methods : Renal electrolyte income and out-lay were determined at room air inhalation, subsequently during 10% O₂ inhalation for 20 minutes by standard renal clearance under simultaneous renal vein catheterization. Sodium and potassium were determined by using flame photometer, Lange 11 type. Subjects: 1) Healthy subjects (Group I, 6 cases): blood pressure below 140/90mmHg, albuminuria(-), PSP (15min.) 25 to 35% ; K.W. 0 degree. 2) Pulmonary tuberculosis (Group II, 4 cases) : blood pressure below 140/90mmHg; albuminuria (-), PSP (15min.) 25 to 35% ; K.W. 0 to 1 degree. 3) Essential hypertension (Group III, 7 cases) : blood pressure 168∼184/95∼136 mmHg. ; albuminuria (-), PSP (15min.) 20 to 30% ; K.W. IIa to IIb degree. 4) Nephrosclerosis (Group IV, 4 cases) : blood pressure 170∼194/96∼106 mm Hg; albuminuria (-); PSP (15min.) 15 to 17% ; K.W. IIb to III degree; 21 cases in total. In the following, the results are described in the above mentioned order, with the means for each group. Results A. Renal electrolyte metabolism during room air inhalation. 1) Plasma level (mEq/L). Na: 139.7, 136.8, 136.7, 137.8. K: 3.6, 3.6, 3.5, 3.1. 2) Filtration amount (μEq/min). Na: 17110, 15452, 15624, 11567. K: 445, 401, 403, 267. 3) Reabsorption amount (μEq/min). Na: 16544, 15143, 14927, 11287. K: 367, 249, 313, 183. 4) Urinary excretion (μEq/min). Na: 582, 309, 691, 285. K, 53, 53, 75, 65. 5) Renal clearance (cc/min). CN_a: 4.2, 2.3, 5.1, 2.4. CK: 14.6, 14.9, 21.9, 23.7. 6) CK/CN. : 3.5, 8.7, 4.5, 10.1.

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