BUBBLE-INDUCED AGGREGATION OF PLATELETS - EFFECTS OF GAS SPECIES, PROTEINS, AND DECOMPRESSION

We show that bubbles containing different gases (N2, He, Ne, Ar, or an O2-CO2-N2 mixture) are equally potent platelet agonists. The synergis tic effect of different platelet antagonists does not seem to be affec ted by the type of gas in the bubbles. In contrast to aggregation in p latelet-rich plasma (PRP), bubbles cause only a weak response in gel-f iltered platelets (GFP), i.e., comparison of aggregation in protein-ri ch and protein-poor platelet suspensions may shed light on the role of different plasma proteins. Extracellular fibrinogen promotes bubble-i nduced platelet aggregation similar to known physiologic agonists, whe reas albumin counteracts this aggregation. Bubble-induced aggregation is inhibited in GFP-fibrinogen by 2-deoxy-D-glucose plus antimycin A, suggesting dependency on ATP generation in the platelets and evidence for direct exposure of the ''cryptic'' fibrinogen receptor by bubbles. Hyperbaric compression and subsequent rapid, inadequate decompression of PRP caused little change in the aggregation response to gas bubble s and epinephrine at 1 bar, but reduced the response to ADP. Bubbles t ended not to form before the surface film was broken. Pressure-induced aggregation was apparently metabolically active and not due to passiv e agglutination; electron microscopic studies and PRP with added gluta raldehyde did not show platelet activation, clumping, or reduced plate let count. In contrast to aggregation caused by pressure, bubble-induc ed aggregation in PRP at 1 bar (after treatment in the pressure chambe r) was nearly completely inhibited by theophylline, a phosphodiesteras e inhibitor that increases intracellular platelet cyclic AMP.