28-day thawed plasma maintains α2 -antiplasmin levels and inhibits tPA-induced fibrinolysis.

Abstract

Evidence supports the use of plasma-first resuscitation in the treatment of trauma-induced coagulopathy (TIC). While thawed plasma (TP) has logistical benefits, the ability of plasma proteins to attenuate fibrinolysis and correct TIC remain unknown. We hypothesize that TP retains the ability to inhibit tissue plasminogen activator(tPA)-induced fibrinolysis at 28-day storage. Healthy volunteers underwent blood draws followed by 50% dilution of whole blood (WB) with TP at 28-, 21-, 14-, 7-, 5-, and, 0-day storage, normal saline (NS), and WB control. Samples underwent citrated tPA-challenge (75ng/ml) thromboelastography (TEG). Plasminogen activator inhibitor-1 (PAI-1) and α2 -antiplasmin (α2 -AP) concentrations in thawed or stored plasma were determined. In the presence of tPA, 28-day TP inhibited tPA-induced coagulopathy as effectively as WB. 28-day TP had a similar R-time, MA, and fibrinolysis (P>0·05 for all) compared to WB, while angle was enhanced (P=0·02) compared to WB. Significant correlations were present between storage time and clot strength (P=0·04) and storage time and fibrinolysis (P=0·0029). Active PAI-1 levels in thawed plasma were 1·10±0·54ng/mL while total PAI-1 levels were 4·79±1·41ng/mL. There was no difference of α2 -AP levels in FFP (40·45±3·5μg/mL) compared to plasma thawed for 14 (36·78±5·39μg/mL, P=0·65) or 28days (45·16±5·61μg/mL, P=0·51). Thawed plasma retained the ability to inhibit tPA-induced fibrinolysis over 28-day storage at 1-4°C. α2 -AP levels were maintained in plasma thawed for 28days and FFP. These in vitro results suggest consideration should be made to increasing the storage life of TP.