ROLE OF LACTATE IN PLATELET STORAGE LESION

It is known that lactate accumulation may cause a pH fall in platelet concentrates (PC) during storage, and this phenomenon causes platelet morphological lesions and loss of platelet in vivo viability. In this study, we added increasing amounts of lactate to identical PC in order to evaluate the role of hydrogen ion accumulation in determining platelet activation and lesion during storage. Six hours after PC preparation, lactate was added to PC1 and PC2 at 20 and 12 mM final concentrations, respectively, while PC3 served as control. In PCI, pH was lower than 6.3, and platelet function and discoid morphology were lost. PC2 were stored for 7 days at pH values ranging from 6.4 to 6.6, and most results of in vitro measurements reflecting platelet function such as osmotic reversal, ATP release and aggregation in response to different stimuli were not significantly inferior when compared to controls. The addition of lactate had no apparent effect on the rise of platelet activation markers P-Selectin, lysosome-like protein gp 53, platelet-bound fibrinogen and granulophysin, while a reduction of borderline significance was observed in glycoprotein Ib expression after pH reduction to values lower than 6.6. It is concluded that the rise of platelet activation markers during storage reflects platelet lesions different from those determined by lactate per se.