AMS (acute mountain sickness), a vascular occlusive disease.
It is hypothesized that a cause of AMS could be vascular occlusion due to hemostatic plugs formed by DIPA (decompression-inducible platelet aggregation). Ex vivo experiments led to the current hypothesis that the rate of fibrin polymerization is accelerated by decompression and decelerated by compression. When experimental pressure is 253 torr (as at the top of Mt. Everest): (1) DIPA takes place independently of PO2; (2) ex vivo DIPA can be inhibited by menthol, thymol, piracetam and pentoxifylline. The experimental design was based on the premise that oppositely charged amino acid residues of adhesive site(s) are juxtaposed. Interaction of oppositely charged residues results in relaxation of electric constriction which causes the volume of the solution to increase. Because of the pressure-volume relationship, decompression alone can induce platelet aggregation. It is concluded that DIPA can be prevented and/or reversed by recompression, and by agents with a large electric dipole moment. It is suggested that the data presented here could be useful for DIPA investigations in vivo toward the prevention and/or alleviation of AMS.
Murayama
M
M
Laboratory of Physical Biology, NIAMS, NIH, Bethesda, Maryland 20892.
D000399:Air Pressure; D000532:Altitude Sickness / Q000097:blood*; D001157:Arterial Occlusive Diseases / Q000097:blood*; D003664:Decompression / Q000009:adverse effects; D006801:Humans; D000860:Hypoxia / Q000097:blood*; D009391:Nephelometry and Turbidimetry; D010100:Oxygen / Q000494:pharmacology; D010974:Platelet Aggregation / Q000502:physiology*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology
D010975:Platelet Aggregation Inhibitors; D010100:Oxygen