PubMed · 3302385
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H Inaba, S Ikematsu. 1987. [Factor XIII].. https://pubmed.ncbi.nlm.nih.gov/3302385/
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Platelet accumulation on small- and medium-calibre vascular grafts plays a significant role in graft occlusion. We examined platelet accumulation on the surface of fibrin-coated polyethylene tubing (internal diameter 0.17 cm) during 10 min flow (10 ml/min) at high wall shear rate (764 s-1). Washed platelets labelled with 51Cr were resuspended in Tyrode solution containing albumin, apyrase and red blood cells (hematocrit 40%). When the thrombin that was used to form the fibrin-coated surface was inactivated with FPRCH2Cl before perfusion of the tubes with the platelet: red blood cell suspension, the accumulation of platelets was 59,840 +/- 27,960 platelets per mm2, whereas accumulation on fibrin with residual active thrombin was 316,750 +/- 32,560 platelets per mm2 (n = 4). When the fibrin on the surface was cross-linked by including recombinant factor XIII (rFXIII) in the fibrinogen solution used to prepare the fibrin-coated surface, platelet accumulation, after thrombin neutralization, was reduced by the cross-linking from 46,974 +/- 9702 to 36,818 +/- 7964 platelets per mm2 (n = 12, p < 0.01). Platelet accumulation on tubes coated with D-dimer was ten times less than on tubes coated with D-domain; this finding also supports the observation that cross-linking of fibrin with the formation gamma-gamma dimers reduces platelet accumulation on the fibrin-coated surface. Thrombin-activated platelets themselves were shown to cross-link fibrin when they had adhered to it during perfusion, or in a static system in which thrombin was used to form clots from FXIII-free fibrinogen in the presence of platelets.(ABSTRACT TRUNCATED AT 250 WORDS)
The new photometric assay described by Fickenscher et al. (Thromb. Haemostas. 65 (1991) 535-540) for the determination of factor XIII facilitates the diagnosis of factor XIII deficiency. In spite of easy handling, this test should be used critically. Patients with hyperfibrinogenaemia showed factor XIII activities of less than 20%, whereas with an optimized assay we found normal factor XIII values. Also, the use of a fixed period of incubation for the analysis is questionable, because the period of constant reaction rate occurs earlier and is shorter with high factor XIII activities and later and longer with low factor XIII activities. A linear relation between factor XIII activity and signal only exists up to 80% of activity. In some plasma samples from patients with hyperfibrinogenaemia the factor XIII determination actually shows decreased values for factor XIII. During the reaction, a fibrin clot is formed. The resulting turbidity simulates an increase in absorbance so that NADH consumption is apparently decreased. In six patients with hyperfibrinogenaemia (8.1-9.4 g/l), a factor XIII activity of 26 U/l or less was determined. Using 50 microliters instead of 100 microliters sample volume, 50% (3/6) of the patients showed a normal factor XIII activities (80-96 U/l), whereas 50% (3/6) values of 6-15 U/l were found. In our modified assay we measured normal factor XIII activities (72-151 U/l) in all 6 patients. The procedure is optimized by reducing the sample volume from 100 microliters to 50 microliters.(ABSTRACT TRUNCATED AT 250 WORDS)
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