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B Dreyer

Publications and source records attributed to B Dreyer.

4 recordsLinked to original sources
PubMed1984

Plasma contact activation and decrease of factor V activity on negatively-charged polyelectrolytes.

The effect of negatively-charged polymers, used in some artificial devices, on plasma clotting and kinin systems was studied in vitro using polyelectrolyte complexes. Contact activation was observed as an immediate, transient and surface-dependent phenomenon. After incubation of the plasma with the polymer a small decrease of factor XII activity was noticed, which corresponded to a greater reduction of prekallikrein activity and to a marked kinin release. No significant decrease of factor XII, prekallikrein, HMW kininogen could be detected immunologically. Only the initial contact of the plasma with the polyelectrolyte lead to activation, subsequently the surface became inert. Beside contact activation, factor V activity also decreased in the plasma. The decrease was surface and time-dependent. It was independent of contact factor activation, and appeared to be related to the sulfonated groups of the polymer. If purified factor V was used instead of plasma factor V, inactivation was immediate and not time-dependent suggesting a direct adsorption on the surface. A second incubation of the plasma-contacted polymer with fresh plasma resulted in a further loss of Factor V activity.

Electrolytes↗
PubMed1980

The collagenous components of the subendothelium. Correlation of structure and function.

Endothelial cells provide a continuous nonthrombogenic lining for the vascular tree. Once the endothelium is denuded platelet adhesion and aggregation occur. One postulated mechanism for the nonthrombogenic properties of the endothelial surface is PGI2 production by endothelial cells, which strongly inhibits platelet aggregation. We propose here that the collagen type(s) associated with the endothelial cell surface may also play an important role in these phenomenon. We found that endothelial cells in culture produce types IV and AB2 collagen (both do not aggregate platelets in vitro) and that type AB2 collagen is uniformly distributed on the endothelial cell surface. We have shown this by immunofluorescence microscopy, immunoelectron microscopy, biosynthetic incorporation, and specific immunoprecipitation techniques. Platelets will not aggregate on monolayers of endothelium while they will aggregate on monolayers of other cells cultured from the vascular wall which produce collagen types that aggregate platelets in vitro. Thus, a specific cell surface-associated collagen (type AB2) may be an important determinant in the ability of the endothelial cell to present a nonthrombogenic surface to the blood.

Animals↗