Compression inhibits aggregation of human platelets under high hydraulic pressure.
It has been found in our laboratory that compression induces disaggregation and decompression induces aggregation of human platelets. The experimental design was based on the premise that oppositely charged amino acid residues of fibrinogen are juxtaposed in the specific adhesive site(s). This can be explained by the principle of Le Chateller. Under compression, electrically charged groups gain layers of water molecules which are radially oriented and pulled in closer to the center of the charge, thus making the layer more compact. This increases the thickness of the shield, thus inactivating or disaggregating the platelets. Conversely, decompression drives the water away from the compact shield; water molecules are randomized into the bulk phase; the shield becomes thinner, thus permitting spontaneous aggregation of platelets. It is well known that increasing the concentration of neutral salt can inhibit platelet aggregation. This is due to the increase of ionic strength which attenuates the electric charge and thickens the shield. Molecules having a large electric dipole moment can inhibit platelet aggregation by a similar mechanism. It is generally accepted that fibrinogen is involved in platelet aggregation. However, it is not known whether or not fibrinogen is essential for platelet aggregation inducible by decompression. Here we present data indicating that fibrinogen is essential in decompression-inducible platelet aggregation. We also present experimental data which show that high hydraulic pressure inhibits platelet aggregation, consistent with our premise that electrically charged groups are involved in the initial phase of platelet aggregation.
D001792:Blood Platelets / Q000166:cytology; D002850:Chromatography, Gel / Q000379:methods; D005340:Fibrinogen / Q000502:physiology; D006801:Humans; D006874:Hydrostatic Pressure; D010974:Platelet Aggregation / Q000187:drug effects; D011312:Pressure
D005340:Fibrinogen