Abstract
Two new findings are presented in this report: (1) it was demonstrated the fibrin monomer polymerization essentially resulted to the paracoagulation of soluble fibrin monomer complex (SFMC) induced by protamine sulfate, histone or some paracoagulants; and (2) it was found that an accelerating and/or inhibiting substance against the fibrin monomer polymerization existed in the bovine arota extract.This study was undertaken to explain an essential phenomenon of paracoagulation induced by basic protein, protamine sulfate or histone, and compare the effects on the paracoagulation and fibrin monomer polymerization due to the variation of pH or ionic strength, and anti-paracoagulants which were acid mucopolysaccharides.The paracoagulants which produce the paracoagulation of SFMC accelerated the fibrin monomer polymerization. Paracoagulation of SFMC and fibrin monomer polymerization identically showed the change with the variation of pH, and were accelerated in the range over neutral pH. Furthermore, as the examination of the effect of ionic strength on paracoagulation and fibrin monomer polymerization, at the low ionic strength they were accelerated and inhibited at the high ionic strength.Anti-paracoagulants, acid mucopolysaccharides, heparin, hyaluronic acid and chondroitin sulfate, inhibited the fibrin monomer polymerization induced by protamine sulfate.From above mentioned results, it was demonstrated that the paracoagulation of SFMC essentially resulted from the fibrin monomer polymerization.This led to further experimentation whether accelerator and/or inhibitor to fibrin monomer polymerization was exist in the bovine arota wall or not.Arota extracts were fractionated with ammonium sulfate to 40, 60, 100% saturation precipitate and 100% supernatant.Among these fractions, it was observed that 40% precipitate accelerated the fibrin monomer polymerization and 100% supernatant inhibited the polymerization.From these results, it was suggested that the fibrin monomer polymerization in the arota was regulated by the accelerating and inhibiting substance on the arota wall.
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