Effects of Pressure and Anesthetics on Cell Membranes and Secretory Processes.
Abstract
Platelet aggregation in response to adenosine diphosphate (ADP), epinephrine, collagen, thrombin, ristocetin and phorbol myristate acetate (PMA) was studied at 1 ATA (air) and 35 ATA (helium) as was platelet shape change. Pressure inhibited aggregation in response to all agents except PMA and it had no effect on shape change. Dose response were constructed for ADP and epinephrine at 1 ATA and 35 ATA in the presence and absence of acetylsalicylic acid (ASA) .00025 M final concentration. With primary aggregation thus isolated, smoother dose responses were obtained and pressure flattened the response in the higher dose range, a behavior suggestive of non-competitive blockade or reduced availability of receptors. All of the agents that were inhibited by pressure are dependent upon extracellular Ca(2 +) for their function. All unmask other receptors (integrins) for adhesive proteins, principally fibrinogen. These integrins incorporate Ca(2 +) to become active. In contrast, PMA aggregation and shape change both are independent of extracellular Ca(2 +) (EDTA was used as a chelator of Ca(2 +) and were unaffected by pressure. It is proposed that pressure distorts Ca(2 +)-dependent surface glycoprotein receptors in a manner that reduces ligand affinity and hence inhibits platelet aggregation. (aw)
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 1989
- Accession Number
- ADA207461
Entities
People
- D. J. Mciver
- R. B. Philp
Organizations
- Western University