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Biomedical subjects

D Collen

Publications and source records attributed to D Collen.

At least 685 records · Page 38Linked to original sources
PubMed1972

Metabolism of plasminogen in healthy subjects: effect of tranexamic acid.

The metabolism of human plasminogen labeled with radioactive iodine was studied in 12 healthy men. The labeled plasminogen had a high specific activity and the same elution on Sephadex G-100 as the plasminogen activity in plasma. Immunoelectrophoresis revealed a single precipitin line. Polyacrylamide gel electrophoresis revealed six main bands, all with plasminogen properties and radioactivity. The purified plasminogen behaved as a homogeneous protein in the turnover experiments. The plasma radioactivity data were adequately approximated by a sum of two exponential terms. The metabolism of plasminogen was therefore represented by a two-compartment mammillary model. Results in the 12 normal subjects were as follows: plasma plasminogen concentration 20.8+/-1.9 mg/100 ml; intravascular plasminogen pool 0.66+/-0.14 g; intravascular fraction 0.59+/-0.06; fractional catabolic rate 0.55+/-0.09 of the plasma pool per day; half-life of the plasma radioactivity 2.21+/-0.29 days. Circulating large-molecular-weight degradation products of labeled plasminogen could not be detected by Sephadex G-100 gel filtration. The plasminogen turnover rate was normal in a patient with Behçet's syndrome and low circulating plasminogen activator activity. This finding supports the concept that under normal conditions the primary pathway of plasminogen catabolism is not via the formation of plasmin. The in vivo effect of tranexamic acid, a potent inhibitor of plasminogen activation, on the turnover of labeled plasminogen was studied in five normal subjects. When 1 g was administered perorally t.i.d. to three of them, one showed an increased plasminogen turnover. A 2 g dose administered t.i.d. to the other two caused markedly increased catabolism in both. This increase may be attributable to a direct reversible effect of tranexamic acid on the plasminogen molecule.

Acrylamides↗
PubMed1971

Metabolism of fibrinogen in cirrhosis of the liver.

The metabolism of human fibrinogen labeled with radioactive iodine was studied in 50 patients with documented cirrhosis of the liver and in 35 healthy control subjects. Results in cirrhotic subjects were the following: plasma volume 47 +/- 10 ml/kg; plasma fibrinogen concentration 250 +/- 102 mg/100 ml; total plasma fibrinogen pool 118 +/- 59 mg/kg, representing 0.73 +/- 0.10 of the total body pool; fibrinogen half-life 2.99 +/- 0.59 days; fractional catabolic rate 0.34 +/- 0.09 of the plasma pool per day; absolute catabolic rate 39 +/- 20 mg/kg per day; fractional transcapillary efflux rate 0.82 +/- 0.30 of the plasma pool per day. Results in the control subjects were the following: plasma volume 42 +/- 7 ml/kg; plasma fibrinogen concentration 284 +/- 71 mg/100 ml; total plasma fibrinogen pool 119 +/- 40 mg/kg, representing 0.72 +/- 0.07 of the total body pool; fibrinogen half-life 4.14 +/- 0.56 days; fractional catabolic rate 0.24 +/- 0.04 of the plasma pool per day; absolute catabolic rate 28 +/- 9 mg/kg per day; fractional transcapillary efflux rate 0.60 +/- 0.26 of the plasma pool per day.A significant difference between cirrhotics and controls was observed for plasma volume, fibrinogen half-life, fractional and total catabolic rates, and transcapillary efflux rate. During heparinization of 10 cirrhotic patients the fibrinogen half-life was prolonged from 3.15 +/- 0.69 to 4.59 +/- 0.79 days. This was associated with a rise in plasma fibrinogen in six out of eight patients. Heparinization did not influence the fibrinogen half-life in five control subjects. Inhibition of the fibrinolytic system in 17 patients resulted in prolongation of the plasma radioactivity half-life of more than 1 day in only three patients, an incidence comparable with that in five control subjects. These results strongly support the concept of accelerated fibrinogen consumption by a process of disseminated intravascular coagulation in cirrhosis of the liver.

Adult↗