The present experiments were carried out to investigate the active center of sodium and potassium ion activated adenosine triphosphatase. An ATPase, activated by sodium ion Plus potassium ion in the presence of magnesium ion, and inhibited by ouabain, has been obtained from rabbit red cell ghosts. The ATPase activity was measured by inorganie phosphate released from ATP. From this values of the measured inorganic phosphate, the activity of ATPase was calculated. The following results were observed. 1. The activity of $(Na^++K^+)-ATPase$ is inhibited by ouabain. This effect may not be due to an effect on sulfhydryl groups, amino groups, carboxyl groups, imidazole groups and hydroxyl groups. 2. The $(Na^++K^+)$-activated enzyme system is inhibited by p-chloromercuribenzoate and by d nitroflurobenzene, and this effect may be due to an effect on sulfhydryl groups. These results indicate that the sulfhydryl groups is attached to sodium-potassium dependent adenosine triphosphate, an aspect of the pump. 3. The $(Na^++K^+)-activated$ enzyme system is inhibited by maleic anhydride and this inhibition is reversed by lysine. This Seems to indicate that the active center of this enzyme is the amino groups. 4. The $(Na^++K^+)$-activated enzyme system is inhibited by iodoacetamide and this inhibition is reversed by the simultaneous present of cysteine and aspartic acid in the suspension medium. This result indicates that this enzyme contains sulfhydryl groups and carboxyl groups. 5. The $(Na^++K^+)-ATPase$ activity is accelerated by adrenaline and this effect is abolished by aspartic acid. This effect of aspartic acid indicate that carboxyl group might be involved in the hydrolysis of ATP by the enzyme system. On the hydrolysis of ATP by the enzyme system. On the basis of these experiments it f·as suggested that the active center of $(Na^++K^+)-activated$ ATPase contains sulfhydryl groups, amino groups and carboxyl groups.

From the study of movements of $Ca^{++}$ in frog cardiac muscle, Niedergerke (1963) postulated that $Ca^{++}$ necessary for the cardiac contraction is stored in a specific pool. Langer et al (1967) and DeCaro (1967) also found a close relationship between the change of $Ca^{++}$ flux kinetics and the change of contractile force. According to the studies of several investigators, Ca II (Bailey and Dressel 1968) or phase I and II (Langer 1965, Langer et al 1967, 1971) in the $Ca^{++}$ washout curve was associated with cardiac contractility. This investigation was aimed to elucidate the anatomical region of the contractile active $Ca^{++}$ pool. At the same time, it was assumed in this study that $Ca^{++}$ in the sarcoplasmic reticulumn represents one of the major intracellular $Ca^{++}$ pool and cardiac contractility was also dependent on the intracellular $Ca^{++}$ concentration. Consequently, this experiment was performed at different temperatures to activate to activate inhibit the deactivating process of activated $Ca^{++}$ in the intracellular space to see if changes in the contractility decay curve existed at different temperatures. The isolated hearts of rabbits and turtles (Amyda maackii) were attached to the perfusion apparatus according to the method employed by Bailey and Dressel (1968). The isolated hearts were initally perfused with a full Ringer solution containing 2 mg/ml of inulin for 1 hr, and then $Ca^{++}$ and inulin-free Ringer solution was perfused while the isometric tension was recorded and a serial sample of perfusion fluid dripping from the cardiac apex was collected for 10 sec throughout experimental period. The above procedure was performed at $23^{\circ}C$, $30^{\circ}C$ and $38^{\circ}C$ on the rabbit heart and $10{\sim}13^{\circ}C$, $10^{\circ}C$, $25^{\circ}C$, $30^{\circ}C$ and $35^{\circ}C$ on the turtle heart. After determination of $Ca^{++}$ and inulin concentration of the samples, the $Ca^{++}$, inulin washout curve and the contractile tensin decay curve were analysed according to the method of Riggs (1963). The results were summarized as follows; 1. In the rabbit heart, there are 2 inulin compartments, 3 $Ca^{++}$ compartments and sing1e exponential decay of contractile tension. In the turtle heart, there are $1{\sim}2$ inulin compartments, $1{\sim}2$ $Ca^{++}$ compartments and $1{\sim}2$ phases of contractile tension decay. The fact that the inulin space was divided into 3 compartments in the washout curve in these hearts indicates the presence of heterogeneity in cardiac perfusion, i.e., overfused and underperfused area. 2. Ca I a9d Ca II in these hearts were found to have $Ca^{++}$ in the ECF compartments because their half times in the washout curves were far smaller than those of the inulin washout curves in the rabbit heart and similar to those of the inulin washout curves in the turtle heart. Ca III in the rabbit heart may have originated from the intracellular $Ca^{++}$ store. But no Ca III in the turtle heart was found. This may be due to the fact that the iutracellular $Ca^{++}$ pool in the turtle heart was too small to detect using this experimental procedure since sarcoplasmic reticulumn in the turtle heart is poorly developed. 3. In the rabbit heart, there were no chages in the half time of Ca I, Ca II, inulin I and inulin II at different temperatures, but the half time of Ca III was significantly prolonged at lower temperatures, and the half time of the contractile tension decay tended to be prolonged at lower temperatures but this was not significant. In the turtle heart, there were no changes in the half time of Ca I, Ca II, inulin 1, inulin II and phase I of the contractile tension decay at different temperatures, but the half time of phase II of the contractile tension decay was significantly prolonged at lower temperatures. This finding indicates that intracellu!ar $Ca^{++}$ in these hearts was also responsible particulary for maintaining the cardiac contractility at the lower temperatures. 4. The half times of contractile tension decay were shorter than those of Ca II in the $Ca^{++}$ washout curves in both animal hearts. According to the above results it was shown that $Ca^{++}$ in ECF is primarily and $Ca^{++}$ in the intracellular space is partially associated with the cardic contractility.

In order to study the dally metabolism of sodium chloride and of nitrogen, 24-hour urine samples were collected from 1,593 normal Korean females whose ages varied from 2 to 80 years old. The volume, the concentration of chloride and the osmolality of the urine, add the total nitrogen were determined, along with the resting pulse rate and the blood pressure. The daily urine volume was maintained at $1,000{\sim}1,300\;ml/m^2/day$ in all age groups while the chloride concentration and osmolality of the urine samples were approximately 200 mEq/liter and 600 milliosmoles, respectively, in most of age groups. Hence the daily urinary output of sodium chloride was estimated to be approximately $15g/m^2$/day in adult groups. On the other hand, the daily excretion of total nitrogen amouted to approximately $5{\sim}6g/m^2/day$. These findings indicated that the average Korean females live on low-protein and high-salt diets throughout their life. Despite a known correlation between the incidence of hypertension and the high salt intake, none of the subjects employed in this work showed any sign of hypertension.

Adult rabbits were anesthetized with nembutal, 30 mg/kg. Carotid artery and jugular vein were exposed surgically and cannulated with polyethylene tubing. Arterial blood pressure was recorded via pressure transducer on the physiograph and $100{\mu}g/ml$ of histamine solution was infused through the jugular vein by using the constant infusion pump with a rate of 0.92 ml/min or 1.40 ml/min. Mean arterial blood pressure was maintained at $40{\sim}70 mmHg$ and hypotension was kept for 2 hours. After the termination of this period, blood was taken and osmotic fragility was mea sured immediately. Also, every sample of normal blood and shocked blood was incubated for 1 hour or 2 hours at $37^{\circ}C$ in order to see whether or not there was some influence of incubation. Furthermore to clarify which component was responsible for the change on the fragility, the mixtures of normal blood cells with shocked plasma and shocked blood cells with normal plasma were also incubated at $37^{\circ}C$ for one or two hours and fragility in such cases was measured. The data obtained were analysed by probit-plot method and the concentration of saline solution at which the hemolysis started to occur, 50% of blood cells were hemolysed and that at which the red blood cells hemolysed completely were determined. The values for the blood of hypotension stage were compared with those of the control blood. The results obtained were as fellows: 1. Osmotic fragility of red blood cell was increased in hypotensive state induced by histamine. 2. The differences of osmotic fragility after two hours of incubation were negligible both in normal blood and in that of hypotensive state. 3. Osmotic resistance of normal red blood cell incubated in shock plasma was less than that of shock red blood cell incubated in normal plasma. It was suggested that plasma in hypotensive state caused by histamine might be primarily responsible for the alteration of red blood cell fragility.

The effects of histamine on cardiovascular system in 6 dogs were analyzed. Mongrel dogs, 10 to 16 kg in body weight, were anesthetized with Nembutal (30 mg/kg) and arterial blood pressure, heart rate, central venous pressure, electrocardiogram were recorded and measured plasma potassium concentration. Histamine $(100{\mu}g/ml)$ was infused slowly at the rate of 0.25 ml/min through the external jugular vein until BP was 80/60 and maintained restored BP for more than 5 min. The process repeated $4{\sim}5$ times. At each time before and after infusion every items were recorded and measured. 1. Arterial blood pressure was 142/105 (mean 117) mmHg in control and decreased to 90/60 68) after histamine infusion. 2. Heart rate changed from 175 beat/min to 150 and central venous pressure from 6.2 to 5.2 cm $H_2O$. 3. Plasma potassium concentration was 4.3 mEq/L and slightly increased to 4.7 mEq/L but it was not significant statistically. 4. Most characteristic changes revealed in EKG especially in T-waves. Height, Width, Steepness, and Slimness were increased $1.5{\sim}3.7$ times than control level and Pointedness decresed 0.5 times than before.

Various factors influencing the lymph flow from thoracic duct were investigated in an attempt to evaluate their contributing degree and the mechanisms. Sixteen mongrel dogs weighing between 10 and 16 kg were anesthetized and polyethylene catheters were inserted into the thoracic duct and femoral veins. Arterial blood pressure, heart rate, central venous pressure, lymph pressure and lymph flow were measured under various conditions. Electrical stimulation of left sciatic nerve, stepwise increase of central venous pressure, manual application of rhythmical depressions onto abdomen, injection of hypertonic saline solution and histamine infusion were employed. Measurement of cental venous pressure was performed through the recording catheter inserted into abdominal inferior vena cava. Changes in central venous pressure were made by an air-ballooning catheter located higher than the tip of the recording catheter in the inferior vena cava. Lymph flow from thoracic duct was measured directly with a graduated centrifuge tube allowing the lymph to flow freely outward through the inserted cannula. The average side pressure of thoracic lymph was $1.1\;cmH_2O$ and lymph flow was 0.40 ml/min or 1.9 ml/kg-hr. Hemodynamic parameters including lymph flow were measure immediately before and after (or during) applying a condition. Stimulation of left sciatic nerve with a square wave (5/sec, 2 msec, 10V) caused the lymph flow to increase 1.4 times. The pattern of lymph flow from thoracic duct was not continuous throughout the respiratory cycle, but was continuous only during Inspiration. Slow and deep respiration appeared to increase the lymph flow than a rapid and shallow respiration. Relationship between central venous pressure and the lymph flow revealed a relatively direct proportionality; Regression equation was Lymph Flow (ml/kg-hr)=0.09 CVP$(cmH_2O)$+0.55, r=0.67. Manual depressions onto the abdomen in accordance with the respiratory cycle caused the lymph flow to increase most remarkably, e.g,. 5.5 times. The application of manual depressions showed a fluctuation of central venous pressure superimposed on the respiratory fluctuation. Hypertonic saline solution (2% NaCl) administered Intravenously by the amount of 10 m1/kg increased the lymph flow 4.6 times. The injection also increased arterial blood pressure, especially systolic Pressure, and the central venous pressure. Slow intravenous infusion of histamine with a rate of 14-32 ${\mu}g/min$ resulted in a remarkable increase in the lymph flow (4.7 times), in spite of much decrease in the blood pressure and a slight decrease in the central venous pressure.

뇌 해마가 전기충격에 의한 내력(tolerance)에 미치는 영향을 구명하기 위하여, 두정 후두 경계 부위의 대뇌피질을 양측성으로 둥글게 떼어내고, 이를 거쳐 해마를 평균 97%가량 떼어버린 흰쥐(해마군) 14마리와 해마를 덮는 대뇌피질 부분만을 떼어버린 흰쥐(대뇌피질 대조군) 17마리 및 두개골을 노출하는데 그치고 뇌에 손상을 주지 않은 흰쥐(정상 대조군) 17마리를 사용하여 다음과 같은 실험을 실시하였다. 24시간 동안 먹이 없이 물만으로 지나게 한 다음 구금판에 세 무리를 구금하고 24시간 동안 매회 1.5초 동안씩 계속되는 4mA의 교류전류에 의한 충격을 1분 간격으로 반복하여 폐사하는 동물의 수효를 세어 다음과 같은 결과를 얻었다. 1. 전기충격을 가하는 동안 폐사한 동물의 수효에서 해마군의 값은 두 대조군의 값에 비하여 유의하게 적었으나, 두 대조군 사이에는 이렇다 할 차가 없었다. 2. 전기충격으로 인하여 폐사한 예에서 전기충격의 시작부터 폐사할 때까지의 시간은 해마군의 값이 두 대조군의 값에 비하여 연장된 경향을 보여 주었다. 이상의 결과로 미루어 뇌 해마는 전기충격에 대한 내력(耐力)에 억제적 영향을 끼친다고 추리된다.

Total body fat measurement by means of skinfold thickness was performed in 295 middle school girls in Suwon, Korea. Skinfold thicknesses on 4 sites, namely, arm, back, abdomen, and waist were obtained and fat was calculated using mean skinfold thickness (MSF) and the following formulas. % Fat=0.747$\times$MSF (mm)+l6.21 Fat (kg) =0.619$\times$MSF (mm) +3.31. The following results were obtained. 1. In 85 (age. 13 yr) of the first year class girls skinfold thickness was: arm 6.9mm; back 8.2; abdomen 8.3; waist 10.7mm, mean thickness was 8.5mm. Fat was 22.6$\pm$1.56% body weight or 8.20±2.68kg. Lean body weight was 31.93$\pm$3.16kg. 2. In 107 (age : 14.2 yr) of the second year class girls skinfold thickness was : arm 7.6mm; back 9.7; abdomen 9.7; waist 12.4mm; and mean thickness was 9.8mm. Fat was 23.0$\pm$5.09% body weight or 9.36$\pm$1.87kg. Lean body weight was 34.29$\pm$1.76 kg. 3. In 103 (age : 15.1 yr) of the third year class girls skinfold thickness was : arm 7.6mm; back 10.3; abdomen 9.4; waist 11.9mm; and mean thickness was 9.8mm. Fat was 23.2$\pm$4.35% body weight or 9.36$\pm$1.18 kg. Lean body weight was 37.10$\pm$5.08 kg. 4. The ratio of mean skinfold thickness (mm) to body weight (kg) was 0.213 in 13 year old girls, 0.225 in 14 year, and 0.213 in 15 year old girls.

Cardiac performances were analyzed in intact turtle heart(Amyda japonica), perfusing with turtle Ringer-Locke's solution containing various hydrogen ion concentration, at several levels of arterial and venous pressure. 1. Ventricular work increased when venous pressure, or venous filling pressure increased, and also increased when arterial pressure increased. 2. The higher the arterial pressure, the lower the cardiac to output, for arterial pressure is the resistance to the ventricular blood flow. On the other hand, in specific arterial pressure, cardiac output was proportional to the venous filling pressure. 3. Heart rates did not change significantly during the perfusion with Ringel· solution of various pH. 4. In the heart Perfused with Ringer solution of various pH, ventricular work was the highest at PH 7.6 (at 6 $cmH_2O$ arterial pressure and 8 $cmH_2O$ venous pressure, the ventricular work was 63.09m$\cdot$cm). However, within the range of pH $7.1{\sim}7.6$, there were no significant changes in cardiac output and ventricular work. Below the level of pH 7.0, ventricular work decreased to less than 56% of maximium value (at $6cmH_2O$ arterial pressure and $8cmH_2O$ venous Pressure, ventricular work was 36.0$gm{\cdot}$ at pH 7.0). At pH 7.7 ventricular work decreased to less than 48% of maximum value (ventricular work: 30.0 $gm{\cdot}$). The nature of the cardiac performance at the various arterial and venous pressures was similar to that of normal heart. 5. Turtle heart seemed to be relatively insensitive to acid-base disturbances. The mechanism of negative inotropic effect of hydrogen ion was discussed.

This experiment was carried out to observe a biological effect of ginseng on the weight gain, physical performance and lactic acid production after exercise in mice. A group of mice weighing about 19 gm was divided into ginseng and cotrol group. on the treadmill (Exp. I & II) and LDH activity of liver and heart homogenates (Exp. II) were determined. Results are summerized as follows; 1. Body weight gain was greater id ginseng group than in control and the difference was statistically significant at 9th and 16th days of experimental period. 2. Maximal running time of ginseng was found to be longer than that of control (p<0.05) in experiment I and the experiment II also revealed the significant increase in maximal running time in ginseng group. 3. Bloo lactate concentration of 48 hour-rest from physical exertion was lower in ginseng group than in control (p<0.05). 4. LDH activity in liver homogenate was lower compared to control group, but in heart homogenate, it was greater in ginseng group. Above findings may be concluded tat the range of biological dose (20 mg/mice/day) of ginseng powder stimulated the body weight gain and increase of physical performance and its mechanism might be attributable to a lower level of blood lactic acid. The adaptive change of LDH activity also contributed to the change in lactate level in blood and tissue.