The purposes of the present study were to: 1) determine whether fibrinogen (Fg) is the plasma protein responsible for spontaneous echo contrast (SEC), and 2) investigate modulators of SEC.
Spontaneous echo contrast has been linked to the development of thromboemboli. The blood products and their interaction responsible for SEC formation have not been fully elucidated.
Blood echogenicity was examined with the use of quantitative videodensitometry over a controlled range of flow velocities in an in vitro model. Human blood samples were analyzed in a manner to methodically eliminate individual blood components from whole blood to determine which components are responsible for the formation of SEC.
The videodensity (VD) of whole blood was found to be flow-dependent, with higher VD at lower flow rates, and correlated with visually dense SEC. The following blood products produced faint VD values: washed red blood cells (wRBCs), platelet-depleted plasma, Fg, defibrinated plasma, wRBCs plus defibrinated plasma, and physiologic saline. The VD of wRBCs increased incrementally as increasing concentrations of Fg were added. At each hematocrit (Hct) range, as Fg concentration increased, the SEC became denser, and the VD level also increased until a plateau level was reached that was distinct for each Hct. The addition of sialic acid, which inhibits RBC-RBC aggregation, decreased the amount of SEC, even in the presence of Fg.
These results demonstrated that Fg-mediated RBC aggregation may be responsible for SEC generation. Furthermore, a unique stoichiometric relationship exists between Fg and RBC concentrations that is necessary for blood echogenicity.