[Clinical relevance of microaggregates in stored blood]

A survey is given on the clinical relevance of microaggregates in stored blood. Initially the pathophysiology of aggregation led by electrostatic and humoral changes on the surface and membrane of the platelets is presented, and the well known pathomechanisms of embolization as well as the functional pulmonary impact of these emboli are discussed. The ever increasing importance of humoral factors is stressed, the mechanic obstruction of pulmonary capillaries by microaggregates having not that clinical importance as the general opinion in earlier days has been. New therapeutic aspects therefore are mentioned: The blockade of aggregation and the release syndrome by adding aspirin, aprotinin or prostaglandin E 1 to the stored blood, pharmacologically influencing the metabolism of arachidonic acid by inhibiting negative effects of prostaglandins (injecting ibuprofen as inhibitor of thromboxane-synthesis) and stimulating positive prostaglandin effects (infusion of prostacyclin), and finally the application of fibronectin (cryoprecipitates) for increasing the RES-function thus also enhancing the clearance of microaggregates, fibrinogen/fibrin complexes and intestinal serotonin. The latter way only, however, is also clinically feasable. The purely mechanical microfiltration should therefore still be used (3 pints of blood at least, pulmonary damage by trauma, shock or sepsis) and the methods of giving aggregate-poor red cell preparations (buffy coat free or saline washed) should be remembered. For the future one could speculate that more or less complete humoral block might be used in conjunction with a "midi-filtration" (Eckert: 40-100 mu diameter standard blood filter).