Metabolism of autologous fibrinogen labeled with radioiodine by a newly devised method was investigated in 34 patients with such diseases as hemiplegia due to cerebral malacia, ischemic heart disease, mitral stenosis with auricular fibrillation, cancer and diabetes mellitus by using the Atencio's analytic method. The results obtained were compared with those in 8 normal subjects.
(1) Mean intravascular half survival time of ¹³¹I-labeled autologous fibrinogen in 8 normal subjects was 4.07±0.08 days and plasma fibrinogen concentration was 119.0±10.9 mg/ kg of body weight. Analysis of plasma disappearance curve of ¹³¹I-labeled autologous fibrinogen revealed that mean J₁, J₂, J₃+J₄, catabolic flux or interstitial pool size in normal subjects was 0.691/day, 1.987/day, 0.237/day, 28.2mg/kg/day or 41.8mg/kg/day, respectively. Acceleration of clearancnce time of ¹³¹I-labeled autologous fibrinogen and increase in catabolic flux are characteristic pattern in fibrinogen metabolism in the patients with above described diseases.
(2) There was no significant correlation of half survival time or catabolic flux to the following : calcium clotting time of oxalate plasma, plasma prothrombin activity, serum prothrombin activity or plasma fibrinogen concentration.
(3) Metabolism of ¹³¹I-labeled autologous fibrinogen was within normal limits in cases of ischemic heart disease or mitral stenosis with auricular fibrillation complicated with thromboembolism under warfarin treatment.
(4) Relationship between fibrinogen metabolism and hypercoagulable state was discussed.

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Metabolism of ¹³¹I-labeled autologous fibrinogen was investigated in the rabbits with experimentally induced hypercoagulable state and the results obtained were as follows : (1) mean intravascular half survival time of ¹³¹I-labeled fibrinogen injected intravenously was 3.0±0.1 days and plasma fibrinogen concentration was 76.6±3.1mg/kg in 12 normal control rabbits.
(2) Disappearance curve of ¹³¹I-labeled fibrinogen from plasma in these 12 normal rabbits was analyzed by the method described by Atencio. Mean values for such coefficients in fibrinogen metabolism as J₁, J₂, J₃+ J₄ catabolic flux and interstitial pool size were 0.89/day, 1.829/day, 0.37/day, 28.3mg/kg/day and 36. 4mg/kg/day, respectively.
(3) Consumption coagulopathy was developed in rabbits following 3 hours' infusion of 2μ/ml of thrombin solution at a rate of 30ml/kg/hour. Platelet count was decreased and both prothrombin time and celite-activated PTT were prolonged significantly. This 3 hours' thrombin infusion resulted in 50% decrease in plasma fibrinogen concentration, while ¹³¹I-labeled fibrinogen in plasma reduced to one third of the initial level. The discrepancy in decrease in plasma fibrinogen was interpreted by increased production of fibrinogen.
(4) Acceleration of clearance time of ¹³¹I-labeled fibrinogen and increase in catabolic flux were observed in rabbits in rebound hypercoagulable state following either the thrombin infusion or abrupt cessation of warfarin treatment. In these animals prothrombin activity, platelet count and plasma fibrinogen concentration were increased and celite-activated PTT and calcium clotting time were accelerated.
(5) Slight but definite acceleration in metabolism of ¹³¹I-labeled fibrinogen was observed in the rabbits fed with lanolin for one to five months.
From the results obtained, it is concluded that acceleration in fibrinogen metabolism is one of the fundamental findings for hypercoagulable state.

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Congenital heart disease is one of the most important diseases in infancy and childhood. In our department, we have found such malformations in 87 cases of 3950 autopsy cases (corresponding to 2, 3%) during 25 years from 1947 to 1971.
It was described on the anatomical findings of each case and discussed on the pathologic evidence characteristic in the congenital heart diseases.

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At autopsy of congenital heart disease, some considerable points were discussed and the method for examination of congenital heart disease was described.
At dissection, the heart and the lungs should be removed together
If the incision should be made by following the blood flow, the examination of congenital heart disease is not so difficult.

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With increased application of radioactive pharmaceuticals, exposure of patients to radiation has attracted grave attention. Especially when mercuric Preparations are used, the kidney is exposed to a large dosis. To eliminate the radioactive substance as early as possible after receiving diagnostic informations is one of the measures to relieve the patient from radiation injury.
Male dd N mice were used as experimental animals. Tracer doses of various radioactive mercuric preparations were intraperitoneally injected to them, and radioactivity was daily measured for 3 days with animal bodies and their excrements, using the whole-body animal counter, and at 3 days radioactivity of ²⁰³Hg in various organs was determined with the well-type scintillation counter. From immediately after the radioisotope injection, various drugs (in doses varying by toxicity) were given every 24 hours, that is, once daily for 3 days and effects on the retention, excretion and organ distribution of ²⁰³Hg were examined to evaluate the eliminating activities.
Drugs that decreased the retention of ²⁰³Hg-MHP and accelerated its urinary excretion were BAL, mercaptoacetic acid (MAA), 2-mercaptopropionyl glycine (MPG), DL-penicillamine (Pen.) and GSH. Furosemide conversely increased the retention. L-CySH, Rongalite and EDTA elicited no change.
Drugs that were effective for elimination of ²⁰³Hg chlormerodrin were MPG, MAA, and Pen. BAL lowered ²⁰³Hg concentration in the kidney, but elevated it in the liver and brain. GSH decreased ²⁰³Hg in the brain and pancreas, but did not change its amount in the other organs. Furosemide increased ²⁰³Hg in the liver and pancreas. EDTA, DTPA and Rongalite exerted no effect.
Drugs that were effective for eliminatin of ²⁰³Hg-Salyrgan were MPG, GSH, Pen and Rongalite. Furosemide and BAL increased the retention.
All the mercuric compounds were increased in body retention under fasting condition. Effect of eliminating them differed in different compounds.
The distribution and excretion of these mercuric compounds administered s.c. or i.p. into Ehrlich ascites cancer-bearing mice were also examined.

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