During mannitol diuresis urinary potassium excretion increased sharply along with sodium excretion under the influence of a large dose of aldosterone, and it remained almost unchanged after 3 days' continuous administration of spirolactone. Plots of potassium excretion rates against sodium excretion rates during ordinary mannitol diuresis without any pretreatment distributed between the 2 extremes. The potassium excretion did not vanish even with spirolactone and at low rate of sodium excretion. This implies that urinary K/Na ratio can take any value at various aldosterone levels in the body, and it offers a poor guide for aldosterone activity without referring correspondent sodium excretion rate.
Since two regression lines representing the effects of aldosterone and spirolactone can contain plots obtained from some other types of diuresis, it is inferred that they present a common mode of renal tubular activity. Sodium in the tubular fluid is suspected to enter the tubular cell and to exchange with potassium there. Aldosterone may enhance this process. This facet of aldosterone activity seems to derange bodily homeostasis for potassium.

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Urinary catecholamines were measured with an attempt for making differential diagnosis of various types of hypertension in which reninangiotensin system is or is not operating. This was based on recent evidences that angiotensin is a potent releaser of catecholamines and aldosterone from the adrenal glands. Twenty patients with essential hypertension, 5 malignant hypertension, 5 renovascular hypertension and 5 primary aldosteronism were subjected to the study. However, no changes in urinary catecholamine excretion were found and all values remained in normal range.
Hypertensive doses of angiotensin infusion to normal men did not alter the output of adrenaline in urine, but did produce a marked decrease in noradrenaline excretion. In rats, intraperitoneal injection of angiotensin induced significant increase in noradrenaline content in the heart, while catecholamine levels in the adrenal glands were remained unchanged after angiotensin administration. Additional experiment showed that infusion of angiotensin to dogs enhanced the blood pressure response to tyramine.
The data indicated that differential diagnosis of hypertension due to primary and secondary aldosteronism was impossible by means of urinary catecholamine assay. With the data obtained from angiotensin treatment in man and in animal, though it was indirect evidence, the authors concluded that there may be an inhibitory mechanism of the sympathetic nervous system in order to adapt to hypertensive state which is produced by angiotensin.

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Lung profile scanning using I¹³¹ labeled macroaggregated albumin (I¹³¹-MAA) was presented as a quantitative estimation of regional pulmonary blood flow. Distribution index in four parts of the lungs (right, left, upper, and lower) was calculated from the area under MAA-pulmogram.
Characteristics of the impaired distribution of pulmonary arterial flow in cardiac diseases were elevation of U/L ratio which consisted of decrease of blood flow in the lower zone associated with increase in the upper zone.
Increased U/L ratio was more characteristic in the patients with left heart failure than with any other specific diseases. From the correlation with hemodynamic variables obtained by the combined right and transseptal left heart catheterizations, increased U/L ratio was found to correlate significantly with left atrial mean pressure. Left atrial mean pressure below 10mm.Hg did not make U/L ratio elevate. When it exceeded 10mm.Hg U/L ratio was observed to increase linearly in proportion to the increased left atrial mean pressure. These facts are well explained by the interstitial perivascular edema of the dependent zone in the isolated perfused dog lung which was first introduced by West et al. in 1965. This external counting technique using I¹³¹-MAA is clinically useful to estimate the severity of various acquired cardiac diseases.

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Lipid and fatty acid composition was studied in plasma and aortic tissue of 6 patients dying of various diseases and in rabbits with experimental atherosclerosis. The atherosclerosis was produced by feeding a lanolin-cottonseed oil mixture diet. On 10th week all rabbits were sacrificed and the aorta removed.
The extracted lipids were separated into esterified cholesterol, triglyceride and phospholipid fractions by multibore column chromatography on florisil. The fatty acid composition of the separated lipids was analysed by gas-liquid chromatography. Results obtained in the present study were as follows :
(1) There were minor differences in the lipid quantity as well as in the percentage distribution in the intima and media. A remarkable increase of total lipid in the plaque was attributed to a corresponding increase in cholesterol and phospholipids. A proportional increase in total cholesterol in the plaque lipid was mainly due to an increase in esterified cholesterol,
(2) There were no significant differences in the fatty acid composition of the cholesterol esters and triglyceride of the plasma, intima or plaque. The phospholipid fatty acid composition of the plaque contained a higher proportion of linoleic and a lower proportion of oleic acid than that of the intima, however these differences between plasma and aortic tissues seemed to be very small. The similarity of the fatty acid composition of the plasma and plaque lipids seems to support the proposition that the plaque lipids are derived from the plasma by filtration.
(3) In the experimental atherosclerosis, the fatty acid composition of cholesterol esters in the plasma of the rabbits fed with the lanolin-cottonseed oil mixture contained a higher proportion of stearic and oleic and a lower proportion of linoleic and arachidonic acids than did the control plasma. There were no significant differences in the fatty acid composition of the triglyceride and phospholipid fractions of the control and lipemic plasma.
(4) The fatty acid composition of the cholesterol esters of the plaquemedia contained a higher proportion of palmitic and oleic and a lower proportion of linoleic acid than that of the intima-media. Similar differences were observed in the triglyceride fatty acid composition, but there was no significant variation in the phospholipid fraction.
(5) After the feeding of the lanolin-cottonseed oil mixture, similar changes in the fatty acid composition of the cholesterol esters were observed in the plasma and aortic tissue ; in both cases there was found a low proportion of polyunsaturated and a high proportion of saturated and monoenoic fatty acids. These results in experimental atherosclerosis seemed also to support the theory of filtration of lipids into the aortic tissue from the plasma.

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Ventricular output curves (left ventricular output vs. left atrial pressure) were studied with coronary arterial pressure controlled at various subphysiological levels in anesthetized dogs. The coronary pressure was changed with a small screw clamp placed around the left main coronary artery, in which a tiny catheter was introduced for coronary pressure measurement. The aortic pressure and cardiac output were controlled at constant values independent of coronary pressure. At low coronary pressures, depression of the plateau and rightward shift of the ventricular output curves was observed. The effect was more marked as the set coronary pressure was lowered. It was concluded that the change in maximal cardiac output (plateau level of the output curve) is a sensitive index of the integrity of cardiac function and that reduction in coronary pressure during hypotensive states plays an important role in the development of vicious cycle of cardiac deterioration. Also observed in the experiment was a consistent correlation between electrocardiographic changes and alterations in cardiac function.

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The activities of myocardial enzyme were determined in heart muscle of normal and hypertensive rats to investigate the changes in cardiac metabolism in the experimentally induced renal hypertension.
In the myocardium under the effect of long-standing hypertension caused by Masugi-nephritis, the activities of G-6-PDH, GAPDH and LDH demonstrated a statistically significant increase, whereas the activities of GK and PFK showed a statistically significant reduction.
In the heart muscle of rats with hypertension induced by Goldblatt's experiment, the activities of G-6-PDH and αGPDH indicated a statistically significant increase, while the activities of PFK, ICDH and MDH demonstrated a statistically significant decrease. The activity of GAPDH showed a tendency to increase.
The changes in myocardial enzyme patterns in the experimentally induced renal hypertension indicate an impairment of oxidative breakdown and increase in anaerobic glycolysis through the pentose monophosphate shunt. These results were well in agreement with the data of previous study on the effect of acute systemic overloading upon the heart and experimentally induced heart failure.
From these deducements, it can be conceived that there is a metabolic defect in the myocardium in experimental hypertension.

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Employing the apparatus which we made of analog computers, spatial velocity electrocardiograms were taken from 321 cases composed of 54 normal cases, 71 cases of left ventricular hypertrophy, 12 cases of right ventricular hypertrophy, 14 cases of complete left bundle branch block, 30 cases of complete right bundle branch block, 10 cases of incomplete right bundle branch block, 41 cases of myocardial infarction and 89 cases of ventricular premature beats. The normal sVECG was composed of 8 chief deflections: π1 and π2 as the counterpart of the P wave of the electrocardiogram, ξ, ρ1, ρ2 and σ as that of the QRS, and τ1 and τ2 as that of the T wave. Normally ρ2 and τ2 were larger than ρ1 and τ1, respectively. In ventricular hypertrophy ξ ρ σ tended to show more splitting and τ to be flatter or the ratio τ1/τ2 was smaller than normal. In left bundle branch block splitting of ξ Ρ σ was most marked and in right bundle branch block σ was wide, frequently making a separate σ'. In myocardial infarction ξ was wide occasionally, and σ was usually wide. ρ1 was often larger than ρ2 in anterior myocardial infarction and was smaller than ρ2 in pos-terior myocardial infarction. τ was variously abnormal in most cases. These and other findings were found useful for diagnosis and the sVECG was found to be especially useful when combined with the vectorcardiogram by effectively supplementing its weak points.

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(1) Clinical data of 197 cases of aortitis syndrome collected by the committee members were analyzed. Their sex and age distribution, past history, chief complaints, changes in arterial pulsation, changes in blood pressure and laboratory data, including arteriographic findings, were demonstrated. The results of medical and surgical treatment were described briefly.
(2) Data of 72 autopsy cases of aortitis syndrome were collected from 29 sources throughout Japan. The antemortem diagnosis and the cause of death in these cases were analyzed, with emphasis that in a considerable number of these cases the presence of arterial disease was not recognized before death. Gross and microscopic findings of the major arteries and their distribution were illustrated.

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Clinical pictures of aortitis syndrome are remarkably manifold. Depending on the site of lesions, many signs and symptoms can grow such as Takayasu's ocular change, pulseless disease, atypical coarctation of the aorta, renovascular hypertension and aortic regurgitation, with several combination in a case. Moreover, occurrence of dilative and aneurysmal changes of the aorta and its main branches in aortitis syndrome has recently been recognized. Two cases of aneurysms in the main branches of the aorta are presented with review of literature. The authors regard them as one of various important manifestations of aortitis syndrome, especially from prognostic and therapeutic standpoints.

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Four surgical cases of the congenital aortic stenosis, that is, a case of the valvular stenosis, a case of the diaphragmatic subvalvular stenosis and 2 cases of the hypertrophic subaortic stenosis, were presented. In Japan, surgical experiences of both the valvular and the paravalvular aortic stenosis have been scarcely reported in the literature. The incidence of these lesions is about l per cent among all operated congenital heart diseases in the Department of the Thoracic and Cardiovascular Surgery of the Niigata University Hospital. Three of them were corrected surgically with success, and a case of the diffuse or idiopathic hypertrophic subaortic stenosis was limited to exploration because its severity was evaluated to be mild.

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