Basophil-derived platelet activating factor (PAF) was shown to induce the release of platelet factor 4 (PF4), a specific platelet protein, from isolated, washed rabbit platelets. The kinetics and dose response of this release were similar to that of PAF-induced 3H-serotonin secretion, and indicated that PF4 release was a reliable and sensitive estimate of platelet stimulation by PAF. Plasma PF4 concentrations were therefore used as a marker for in vivo platelet release during systemic anaphylaxis induced by the i.v. injection of antigen (horseradish peroxidase, HRP) into rabbits conditioned to produce only IgE antibody against HRP. Antigen administration was accompanied by the loss of circulating stainable basophils, acute thrombocytopenia and neutropenia, and a significant increase in PF4 levels. The increase in plasma PF4 began approximately 90 sec after antigen challenge, corresponding to 60 sec after the intravascular aggregation of platelets. However, maximum levels of plasma PF4 were not reached until 3 to 5 min after antigen challenge. Concomitant measurement of circulating PAF during anaphylaxis indicated that PAF release into the circulation preceded the decrease in circulating platelet numbers by about 30 sec and preceded the increase in plasma PF4 levels by about 60 sec. Thus, this study documents that platelets undergo a release reaction during anaphylaxis at a time when they are sequestered in the microvasculature. The temporal relationship of this release suggests that the following series of events occur during IgE anaphylaxis: antigen stimulates circulating IgE-sensitized basophils to release PAF, PAF causes intravascular platelet aggregation and subsequent sequestration, and finally, sequestered platelets release their intracellular constituents.


This work was supported by United States Public Health Service Grants HL 22555 and HL 07350, the Medical Research Service of the Veterans Administration, and the Morrison Trust (R-A-54).

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