Using medical students as controls, we devised a method of quantitative analysis of dermatoglyphic patterns. We calculated the frequency of appearance of each of the patterns and obtained the probability of occurrence of the dermatoglyphics of each of the controls. We showed usefulness of this method by presenting some examples of congenital anomalies where this has been put to use. Furthermore, patients with congential heart disease were compared with controls by this method.

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Measurement of plasma renin concentration (PRC) was done in normal subjects at rest and under acute stimulation of renin release under unrestricted sodium intake. Concurrent measurements of plasma renin activity (PRA) and plasma aldosterone concentration (PA) were carried out. The mean values of PRC at rest and after stimulation of renin release were 12.8 ± 1.3 (SEM) and 21.7 ± 4.4 (SEM) ng AT I/ml/h, respectively. These corresponded to renin contents of 3.4 ± 0.34 (SEM) × 10^-5 Goldblatt units and 5.8 ± 0.36 (SEM), respectively. The mean percent increase of PRC (82.1 ± 19.3 (SEM) %) was almost indentical to that of PA (81.5 ± 16.4 (SEM) %), but differed from that of PRA (269 ± 83.1 (SEM) %). A very high correlation between concurrent PRC and PA (r= 0.92, P < 0.001) was found in normal subjects at rest and under acute stimulation of renin release. A good correlation between PRC and PRA (r = 0.85, P < 0.001) was also observed. However, a higher correlation between percent increases of PRC and PA (r = 0.92, P<0.001) than that of PRA and PA (r = 0.80, 0.01 < P < 0.005) was found. Results show that PRA is a good index of the renin content in plasma in normal subjects at rest and PRC reflects actual renin concentration in plasma at rest as well as under stimulation of renin release.

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Lysosomal fraction of renal cortical extract, which showed high renin activity, and equipressor dosis of synthetic angiotensin II amide were administrated into one-hour nephrectomized rats. Sixty minutes after the sustained elevation of 20 mmHg in mean arterial pressure by each pressor substance, the rats were sacrificed and the intraperitoneal organs were fixed. Five minutes prior to the administration of each pressor substance ferritin solution, as a test substance for vascular permeability, was intravenously injected. Medial changes in the arterioles in the intestinal submucosa were observed by electron microscopy. In angiotensin II group early lytic lesions of the muscle cells were limited to the single muscle cells. Ferritin particles were rarely found in the media. In lysosomal fraction group the lytic lesions were more advanced. Some regions of the media exhibited focal loss of smooth muscle cells manifesting focal medial necrosis. Ferritin particles were distributed in some areas of the necrotic media. The results suggested that the kidney extract with high renin content contained substance(s) to produce both medial necrosis and plasma insudation into the media of the arterioles.

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The present study was performed to investigate whether blood pressure of salt-loaded rats was influenced by the diet. Salt-loaded rats of Wistar strain were fed a high portein high fat diet or a high carbohydrate diet from the age of one month. The experiment was designed so that the intake of sodium chloride was equal in two groups. The body weight on the 14th week of the experiment was 394 ± 15 g (Mean ± SE) in the high protein high fat group, and 348 ± 13 g in the high carbohydrate group. Blood pressure measured weekly by a tail plethysmographic method rose gradually and reached 176 ± 5 mmHg (Mean ± SE) on the 14th week in the high carbohydrate group. It was significantly higher than that (127 ± 7 mmHg) of the high protein high fat group. The pressor responses to angiotensin and noradrenalin were also examined to investigate the mechanism through which salt hypertension was produced more easily by feeding a high carbohydrate diet. These reponses to both drugs tended to be greater in the high carbohydrate group, but the difference between the two groups was not significant.

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[1-Sarcosine, 8-Isoleucine] angiotensin II was given to 8 patients with cirrhosis and ascites and 7 cirrhotic patients without ascites on a regular diet. The 3 ascitic patients with high plasma renin activity (PRA) gave a depressor response, but the other ascitic patients with normal or low PRA gave a pressor response or no response. All the non-ascitic patients gave a pressor response. There was an inverse correlation between the PRA before infusion and the change in blood pressure induced by this compound. In the patient with the highest PRA, who had ascites of a few days' duration, a marked reduction in blood pressure was observed on infusion of this compound. These results suggest that the renin-angiotensin system might be involved in maintenance of a normal blood pressure in some patients with cirrhosis and ascites, whose ascites is presumably in an early stage.

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In order to investigate the regulatory system of release and excretion of ADH in essential hypertension, plasma and urinary ADH levels were determined in normal control subjects and patients with essential hypertension. Plasma ADH levels in 42 normal subjects and 53 patients with essential hypertension were 4.5 ± 0.18 pg/ml (mean ± SEM) and 4.0 ± 0.12 pg/ml, respectively, and a significant difference was found between the two groups. Urinary ADH excretion was 74.4 ± 9.5 ng/day (mean ±SEM) and 48.0 ± 8.2 ng/day in 15 normal subjects and in 17 patients, respectively, and it was significantly lower in the patient group. In 25 patients, plasma ADH levels were measured immediately upon admission and after a two week bed rest without medication following admission. A significantly negative correlation was observed between the change of mean blood pressure and plasma ADH levels. After two weeks, sodium restriction (Na : 35 mEq and K : 75 mEq, daily) was ordered for 1 week in 17 patients, and a significant elevation of plasma ADH levels and a remarkable lowering of the blood pressure was found. And there was also a significantly negative correlation between the change of mean blood pressure and plasma ADH levels. Since the linear regression line was steeper after sodium restriction than after a two week rest, the elevation of plasma ADH levels induced by sodium restriction may be considered to be affected not only by the blood pressure lowering but also by the decrease of plasma volume. From these results, it was suggested that the control of ADH release in essential hypertension was maintained normally, and that the baroreceptor might play an important role in regulation of ADH release under these conditions.

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In this study, an attempt was made to determine if the electrocardiogram (ECG) or vectorcardiogram (VCG) might show previously unrecognized evidence of myocardial infarction, particularly diaphragmatic infarction, in the presence of complete left bundle branch lock (LBBB). ECGs and VCGs of 12 patients with LBBB and diaphragmatic infarction were compared to ECGs and VCGs of 10 patients with LBBB and no infarction. Diaphragmatic infarction was diagnosed on the basis of a typical history and inferior surface perfusion defect on Thallium-201 imaging. The presence of a qR complex in II, III, or aVF irrespective of the size of the q wave, appeared specific for infarction, but identified only 5 of 12 (42%). In contradistinction, a QS complex was nonspecific. Since we found q waves in II, III, or aVF not in 5 patients with left axis deviation but in 5 of 7 patients without it, we would like to suggest the possibility that the presence of left axis deviation is a factor which causes the q waves in the inferior leads to be unnoticeable. A diminished maximum spatial vector of 1.59 mv or less identified infarction (not necessarily diaphragmatic only) also in 5 of 12 (42%). In the frontal plane, a 0.04 sec QRS vector &les; 0.4 mv identified diaphragmatic infarction in 6 of 12 (50%), and in the left sagittal plane, a ratio of the magnitude of the ST vector to the magnitude of the maximum T vector &gas; 0.35 indentified a diaphragmatic infarction in 8 of 12 (67%).

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A 23-year-old Japanese male with no evidence of previous heart disease was presented with bicuspid aortic valve and a life threatening acute aortic regurgitation due to subacute bacterial endocarditis. By echocardiographic techniques, a precise diagnosis was made based on the following findings: 1)premature mitral valve closure, 2) snowfall-like echoes between the systolic aortic cusps, 3) eccentricity of a diastolic aortic valvular echo. The echocardiographic diagnosis was confirmed on surgery, in which aortic valve replacement was performed with satisfactory postoperative results.

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