Abstract. The nature of platelet lesion occurring with storage of platelet concentrates (PC) in second‐generation containers was investigated using various storage media and storage periods up to 14 days. In CPD‐plasma (control medium), the changes which occurred progressively during storage were loss of discoid shape, microscopic platelet aggregate formation, fragmentation and the appearance of disintegrated, ‘balloon’ forms. By day 14 less than 10% of the platelets were discoid in shape, the platelet count had decreased by 23%, and there was a 5‐fold increase in the amount of lactate dehydrogenase in plasma. Associated with this was a decrease in the platelet oxygen consumption rate, D(O2), loss of cellular ATP and extent of ADP‐induced shape change, and a decrease in the hypotonic shock response. These parameters decreased at a similar rate, with a 50% decrease (t1/2) at days 7–9. They correlated highly with each other during storage and also with a fall in pH. At day 14 of storage, mean pH was 6.1 ± 0.3. To evaluate the effect of pH stabilization during storage, 4 mEq sodium bicarbonate was added to PC in CPD‐plasma. Although pH maintenance was much improved, 7.2–6.6 during 14 days of storage, the same in vitro lesions developed, although more slowly. The t1/2 of the same parameters was prolonged for approximately two days. When PC were stored in a plasma‐free physiologic salt solution whose salt composition was similar to CPD‐plasma, the t1/2 of the parameters increased to 11–15 days of storage, although the platelets eventually developed the same in vitro lesions. In all media there was a high correlation between platelet ATP level and the other in vitro parameters during storage. Furthermore, energy depletion of the platelets produced by using the physiologic salt solution without glucose and by addition of metabolic inhibitors caused a similar deterioration of in vitro functions, but at a significantly faster rate which correlated with the rate of decrease in platelet ATP. This suggests that the platelet lesion observed with prolonged storage in second‐generation containers might be due to a failure in platelet energy metabolism.
Vox Sanguinis – Wiley
Published: Nov 1, 1987
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