By the Cabaud method, SGOT was determined chiefly with inpatients in the Shibusawa surgery clinic and experimental animals.
In acute myocardial infarction, SGOT remarkably increased, attaining the maximum at 24 hours. In fresh infarction, SGOT value was proportional with the extent involved by infarction, and above 200 units indicated unsatisfactory prognosis.
Concerning hepatic diseases, up to 2, 000 units was shown in hepatitis, 20, 000 units in intoxication, and 300 units in regressive degeneration. In carbon tetrachloride intoxincation, SGOT value was approximately proportional with in jury of hepatic cells. Histologically, correlation between centrilobular zonal necrosis and SGOT was confirmed. SGOT is a good index for the degtee of destruction of hepatic cells. The administration of 200 mg of cortisone was highly effective for chronic hepatitis, rapidly restoring SGOT to the normal value.
When the elevation of alkaline phosphatase level was due to bone disease, SGOT did not rise, but when it was due hepatic disease, SGOT rose.
In extrahepatic occulusivc icterus, SGOT showed slight rise. When it was surgically removed, SGOT returned to the normal value in 12 weeks.
SGOT can be used for the differentiation between icterus, liver cirrhosis, liver tumor and extrahepatic occulusive icterus.
There is gross correlation between surgical operation and SGOT. In the operation of the chest, cardiac vessel, and bile duct, and in severe wound, remarkable rise in SCOT was observed. Excepting these cases, only slight and transient rise of SGOT was noted.
Rise in SCOT was observed in experimentally produced infarction of the heart, lung, spleen, intestine, kidney and liver.
Relation of SGOT to g-6-pase, aldolase, amylase, alkaline phosphatase, blood ammonium and serum irou was sought.
Determination of liberated glucuronic acid was performed after the Ishidate-Nakajima's method using ion exchange resin, In hepatic diseases, bound glucuronic acid in blood showed greater increase than free one.
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