Plasma oncotic pressure and blood water content were studied clinically from the viewpoint of edema pathogenesis. The conclusions were as follows: 1) Three components of oncotic pressure, namely, true oncotic pressure of protein particles, Donnan's pressure and pressure from swelling of protein colloids were studied theoretically. Also isolation of human plasma albumin and γ-globulin were performed by Howe's method and equations for calculating the oncotic pressure of each collid were established, namely A=36x1.33 for albumin and G=6x1.60 for γ-globulin. (x: concentration of colloids gm/dl) 2) Clinical studies of 186 cases suffering from diseases producing edema (such as heart disease, renal disease, liver disease, anemia, carcinoma etc.) have been carried out, especially concerning edema pathogenesis. Most conspicuous changes of blood water content have been shown in the cases of heart disease, nephrosis and anemia, namely in the cases of heart disease both plasma and corpuscle water were moderately increased, and in the cases of nephrosis remarkable increase of plasma water was present but not in corpuscle water. However in the cases of anemia, water content of corpuscle was only increased without the accompaning increase of plasma water. Oncotic pressure of plasma of such cases was also studied in its relationship with the plasma protein concentration and its fractions. Most remarkable decrease of oncotic pressure, plasma protein and albumin level has been shown in the cases of nephrosis, also remarkable decrease of oncotic pressure with normal plasma protein concentration but with low albumin and high γ-globulin level has been shown in the cases of liver cirrhosis. 3) General relationship between plasma oncotic pressure and concentration of protein fractions was studied and a new equation for calculating the oncotic pressure from the concentration of plasma protein fractions has been established and examined, namely. P=90(Al+1/3α-gl+1/4γ-gl)-75
1. Statistically significant positive correlation was recognized between the mortalities from liver cirrhosis and the mean annual temperatures in the prefectures of Japan. In the countries of the world significant correlation was present only in the countries of mean annual temperature below 16°C. 2. Rats were fed with a choline-deficient diet without cystine at temperature of 7°C and 22°C. On a high fat diet, the liver fat content of the rats which were kept at 7°C was significantly less than that of the rats which were kept at 22°C. At lower temperature food and protein intake increased. The prevention of deposition of liver fat was not observed in the rats which were kept at 7°C, when their protein intake was decreased to the same level as that of the rats which were kept at 22°C. Hence the prevention of deposition of liver fat at lower temperature seemed to be due to the increased protein intake. 3. The liver fat content of the mice which were fed with a cholinedeficient diet with added cystine at temperature of 6°C, 13°C, 19°C, and 26°C increased markedly. No regular relationship between liver fat content and environmental temperature was observed in these animals. 4. The influence of nutrition on the production of liver cirrhosis due to carbon tetrachloride was investigated. With the administration of carbon tetrachloride liver collagen content increased significantly and serum albumin concentration decreased significantly. Protein, choline, and α-tocopherol had no influences on the changes of liver collagen content and serum protein. On a low protein diet fibrosis of the liver which was estimated histologically was reduced by the supplement of α-tocopherol, but not influenced by the addition of choline. Fibrosis of the liver of the rats which were fed with a high protein diet was more advanced than that of the rats which were fed with the low protein diet.
This is a clinical report on an outbreak of an acute arsenic poisoning due to soy-sauce accidentally contaminated by arsenic, which occurred among a population of the City of Ube, Yamaguchi Prefecture, in January 1956. The main symptoms observed in 220 cases out of the total 417 patients were edema of the face, gastrointestinal and upper respiratory symptoms followed by skin lesions and neuritic signs which occurred in a limited number of patients in the late stage. In the majority of patients, the symptoms appeared 2 days after the intake of arsenic and subsided gradually after the 5th or 6th day of illuess, despite continuous intake of the poison. Those symptoms disappeared rapidly after two weeks when the patients ceased taking arsenic, except neuropathy such as abnormal patellar reflex and tenderness in the calf muscle which were aggravated afterwards. The liver was palpated for one or two finger breadths in most of the cases, and decreased in size after the symptoms subsided. Electrocardiogram revealed abnormalities in Q-T interval and P- and T-waves. Ophthalmoiogically, conjunctivitis, central scotoma and neuro-retinitis were detected. Laboratory data indicated; slight anemia, leukopenia, relative lymphocytosis, positive urine urobilinogen in 60 to 80% of the cases, normal electrolytes and ureaclearance. Fecal occult blood was positive in many of the patients, and in some, occult blood was demonstrable in gastric and duodenal juice. Chemical analysis of serum was suggestive of slight involvement of the liver, whereas the biopsy revealed slight but definite degenerative changes such as decrease of nucleic acid in liver cells. Liver detoxifying function was impaired in about half of the cases, but BSP test remained normal. Arsenic was demonstrated in the urine in an appreciable concentration even two weeks after the suspension of arsenic ingestion. A low concentration of arsenic was also detected in both gastric and duodenal juice. The root portion of the hair contained more arsenic than the rest of the hair. The duration of arsenic ingestion was two or three weeks in most of the cases, and arsenic content of the soy-sauce which caused this accident was estimated to be about 0.1mg per milliliter. (The English original report will be presented in the Bulletin of the Yamaguchi Medical School.)