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Human blood platelets in ACD plasma were stored in sterile plastic bags for 24–96 h at the ambient temperature without agitation. No spontaneous aggregation nor bacterial contamination were noted. A progressive loss of the following parameters was seen: platelet count; ADP-, thrombin-, collagen-, and epinephrine-induced platelet aggregation; platelet factor 3 activity; reversible response to the osmotic shock; volumetric constants; amount of UV-absorbant material; ¹⁴C-5-hydroxytryptamine and ³H-adenosine uptake and release; platelet population pattern and glycogen synthesis activity. The platelet aggregation and release, the osmotic shock test, and the platelet population pattern appear to better illustrate the early changes during platelet storage and to account for the 25–42% of recirculation of 24 h stored platelets administered into thrombocytopenic patients. As stated by Murphy and Gaardner, platelets stored at 20–22 °C with or without agitation, although having failed to retain total functional and biochemical capacities, paradoxically seem to recuperate in vivo as shown by survival data and hemostatic effects.

The influence of the salts of saturated and non-saturated fatty acids from C8 to C22 on the aggregation of human platelets is compared within the framework of 2 different techniques: the test of filtration pressure, in correlation with the classical photometric test of aggregation. Thus, with the technique of filtration pressure of platelet-rich plasma, one finds an increase in filtration pressure as a function of the number of carbon molecules in the chain used. The presence of a double bond generally results in a decrease in filtration pressure. In the classical photometric test the fatty acids induce a progressive and irreversible deviation curve, demonstrating both the aggregation of platelets and the probable bonding of the fatty acids with plasmatic proteins. The presence and intensity of platelet aggregation are related to the molecular weight of the chain of fatty acids under consideration and inhibited by the presence of double bonds. From the similarity of the results obtained with the 2 techniques, one might surmise that the filtration pressure test is a new approach to platelet aggregation.

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We studied ultrastructural changes in platelet aggregation induced by fatty acid (FFA) salts. The platelets were used either directly in their original plasma or separated from plasma proteins by washing or filtration on 2 B Sepharose gel and suspended in a buffer solution with or without albumin.After fixation for electron microscopy the aggregating FF A salts appear as micellar structures or spherules of large size ressembling liposomes.During the first seconds of contact between the platelets and the FFA salts we observed the spreading of platelets on the surface of the structures formed, and the particles smaller than 1 μ were phagocytized. After a few minutes platelet release occurred followed by total degranulation of platelets during the formation of aggregates. After eight minutes the aggregates still contain FFA salts structures.These results confirm our earlier views that the mechanism of FFA salt induced aggregation differs from that of aggregation by other agents, and could be due to the micellar structure.