The main thrust of the laboratory is focussed on the influence of pressure on the blood coagulation system, including both hemostasis and thrombosis. The molecular mechanism of platelet interactions in DIPA (decompression-inducible platelet aggregation) has been investigated for the past several years and is still continuing. We have found that the molecular mechanism of DIPA can be explained by the interactions of oppositely charged amino acid residues, i.e., positively charged arginyl residues interact with negatively charged aspartyl residues. We found this to be the molecular mechanism in AMS (acute mountain sickness); vascular occlusion has been observed in the small blood vessels in the web of the frog's foot and in the ear of the mouse. Photomicrographs were made showing platelets adhering to each other and to the blood vessel wall. We found that AMS can be prevented in the frog and in the mouse by the drug piracetam, administered by stomach tube prior to simulated ascent. At the beginning of the project I had assumed that DIPA is accompanied by a volume increase and that there is a neutralization of positive and negative charges. The measurement of this increment is now being determined by using a specially constructed volumetric flask. The experimental findings of the past year confirmed our hypothesis that AMS is a vascular occlusive disease.
