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AMS (acute mountain sickness), a vascular occlusive disease
1Laboratory of Physical Biology, NIAMS, NIH, Bethesda, Maryland 20892.
Medical Hypotheses
|March 1, 1990
Summary
Decompression-inducible platelet aggregation (DIPA) may cause altitude sickness by forming vascular plugs. This process can be prevented or reversed by recompression and specific agents.
Area of Science:
- Physiology
- Biophysics
- Altitude Medicine
Background:
- Altitude sickness (AMS) may stem from vascular issues.
- Decompression-inducible platelet aggregation (DIPA) is a potential cause of vascular occlusion.
Purpose of the Study:
- To investigate the mechanism of DIPA.
- To identify potential preventative or therapeutic agents for DIPA and AMS.
Main Methods:
- Ex vivo experiments simulating high-altitude pressure (253 torr).
- Investigated DIPA's independence from PO2.
- Tested inhibition of DIPA by menthol, thymol, piracetam, and pentoxifylline.
Main Results:
- Decompression accelerates fibrin polymerization, while compression decelerates it.
- DIPA occurred independently of oxygen partial pressure (PO2) at 253 torr.
- Menthol, thymol, piracetam, and pentoxifylline inhibited ex vivo DIPA.
Conclusions:
- Decompression alone can induce platelet aggregation due to pressure-volume changes.
- DIPA can be prevented or reversed by recompression and agents with large electric dipole moments.
- Findings may aid in vivo DIPA investigations for AMS prevention and alleviation.