After diving, in decompression sickness and after extra-corporeal circulation in membrane
oxygenators, there is often a reductionin the number of circulating platelets. Gas
bubbles seem to be the common denominator for these quite different conditions, and
it is assumed that gas bubbles activate the platelets although by unknown mechanisms.
We have used gas bubbles as a platelet agonist in an aggregometer-like apparatus.
The bubbles produced platelet aggregation similar to that caused by "classical" agonists,e.g.,ADP,
epinephrine etc. The gas-liquidinterface was essential for this aggregation,and the
bubble diameter, rather than thetype of gas or the total number of bubbles, determined
the potency of this agonist. Electron microscopical studies revealed that singleplatelets
and platelet aggregates with numerous, short pseudopods adhered to the bubble wall.
The platelet aggregation caused bygas bubbles was abolished by metabolic blockers
(2-deoxyglucose and antimycin A), EGTA,phosphodiesterase inhibitors (theophylline,
caffeine, papaverine, dipyridamole), adenylate cyclase activators (PGE1 adenosine, AMP), or a combination of low concentrationsof phosphodiesterase inhibitors
and adenylate activators. Theophylline which is regardedas a weak inhibitor of platelet
activation in general, was an especially potent inhibitor of gas bubble-induced platelet
aggregationwhereas cyclooxygenase inhibitors (acetyl salicylic acid, indomethacin),
adrenoreceptor blocker (yohimbine), guanylate cyclase activators (azide, jiitroprusside)
and trifluoperazine had little or no effect. Bubble-induced,aggregation is thus similar
to theprimary,and not the secondary, aggregation caused byclassical agonists. However,
the ineffectiveness of guanylate cyclase activators distinguishes bubble-induced aggegation
from "classical" primary aggregation.
