The main thrust of the laboratory is focused on the molecular mechanism of platelet aggregation, including both hemostasis and platelet aggregation inducible by decompression (both by reduced barometric and hydrostatic pressure). We are investigating the influence of change of pressure on the hydration layer surrounding the electrically charged amino acid residues involved in platelet aggregation. We have been investigating the molecular mechanism of platelet interactions in DIPA (decompression-inducible platelet aggregation) for the past several years. We have found that oppositely charged amino acid residues interact with their respective receptor sites. We have observed vascular occlusion in the small blood vessels in the web of the frog's foot and in the ear of the mouse. During the current year we have confirmed that the volume of human PRP is increased by 0.3% or 3 ml per liter of packed thrombocyte volume when platelet aggregation is induced by decompression. A similar volume increase has been observed when platelet aggregation is induced by the agonist, epinephrine (adrenalin), ADP, collagen and PAF (platelet activating factor). We theorize that compactly organized water molecules, when randomized into the bulk phase, acquire thermal motion which causes plasma volume to increase and a temperature drop; and that human platelet aggregation is an entropy driven process similar to human red cell sickling. To confirm our hypothesis, we are continuing our experiments with a specially designed dilatometer, including a thermistor, to measure the volume increase and temperature drop when platelet aggregation is induced by the agonists epinephrine, ADP, and PAF. During the year we have obtained additional confirmation of volume increase of human plasma due to decompression by using the discontinuous, density gradient zonal centrifugation method.
