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The Effect of the Fibrinogen Concentration and White Cell Count on Intravascular Fibrin Deposition
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The relationship between blood fibrinogen concentration and intravascular fibrin deposition was examined in EACA-treated rabbits infused with a standard amount of thrombin or simplastin sufficient to produce fibrin monomer (FM) but not defibrination. Fibrin in organs was measured by a previously described quantitative technique using 125I-fibrinogen. A significant (p<0.01) positive correlation was found between the baseline fibrinogen concentration and fibrin deposition 3 hours after infusion. By contrast, in vitro there was an inverse relationship between fibrinogen concentration and enzymatic clotting as well as non-enzymatic fibrin formation from soluble FM. When HN2-treated leukopenic rabbits were infused, fibrin deposition was inhibited despite the fact that the animals’ fibrinogen concentration was substantially increased by the HN2 treatment. When leukocytosis was induced by pretreatment with endotoxin, fibrin deposition was potentiated. It is concluded that fibrin deposition from circulating FM is facilitated by a raised fibrinogen concentration by a mechanism that cannot be explained by the well known in vitro interaction between FM and fibrinogen. Secondly, white cells appear to participate in the intravascular precipitation of circulating soluble FM complexes.
Title: The Effect of the Fibrinogen Concentration and White Cell Count on Intravascular Fibrin Deposition
Description:
The relationship between blood fibrinogen concentration and intravascular fibrin deposition was examined in EACA-treated rabbits infused with a standard amount of thrombin or simplastin sufficient to produce fibrin monomer (FM) but not defibrination.
Fibrin in organs was measured by a previously described quantitative technique using 125I-fibrinogen.
A significant (p<0.
01) positive correlation was found between the baseline fibrinogen concentration and fibrin deposition 3 hours after infusion.
By contrast, in vitro there was an inverse relationship between fibrinogen concentration and enzymatic clotting as well as non-enzymatic fibrin formation from soluble FM.
When HN2-treated leukopenic rabbits were infused, fibrin deposition was inhibited despite the fact that the animals’ fibrinogen concentration was substantially increased by the HN2 treatment.
When leukocytosis was induced by pretreatment with endotoxin, fibrin deposition was potentiated.
It is concluded that fibrin deposition from circulating FM is facilitated by a raised fibrinogen concentration by a mechanism that cannot be explained by the well known in vitro interaction between FM and fibrinogen.
Secondly, white cells appear to participate in the intravascular precipitation of circulating soluble FM complexes.
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