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Evaluation of adenosine, lidocaine, and magnesium for enhancement of platelet function during storage
James A Bynum1, Ashley S Taylor, Grantham C Peltier
1From the US Army Institute of Surgical Research (J.A.B., A.S.T., G.C.P., C.S.M., M.A.M., A.P.C.), JBSA-Fort Sam Houston, TX,; Heart, Trauma & Sepsis Research Laboratory, Australian Institute of Tropical Health and Medicine, College of Medicine and Dentistry, James Cook University, Townsville, Queensland, Australia (G.P.D).
Background:
The combination of adenosine, lidocaine, and magnesium (Mg2+) (ALM) has demonstrated cardioprotective and resuscitative properties in models of cardiac arrest and hemorrhagic shock that are linked to reduction of metabolic demand. Platelets play a key role in resuscitation strategies for ATC but suffer from loss of function following storage in part owing to mitochondrial exhaustion. This study evaluates whether ALM also demonstrates protective properties in stored platelet preparations.
Methods:
Platelets were tested at (baseline, Day 5, Day 10, and Day 15) at 22°C (room temperature) or 4°C in 100% plasma and platelet additive solution. Adenosine, lidocaine, and magnesium treatment or its individual components (A, L, M, or combinations) were added directly to the minibags at baseline for storage. Measurements consisted of blood gas and chemistry analyses, thromboelastography, impedance aggregometry, and flow cytometry.
Results:
Blood gas and cell analysis, as well as flow cytometry measures, demonstrated only differences between temperature groups starting at Day 5 (p < 0.05) and no differences between treatment groups. Aggregation response to collagen (A only, M only, and ALM high dose) and thrombin receptor activation peptide (A + M, and ALM high dose) was significantly greater at Day 5 compared to respective 4°C (100% plasma) controls (p < 0.05). Thromboelastography analysis revealed significant preservation of all measures (reaction time, maximum amplitude, and angle) at Day 15 for 4°C-stored samples in 100% plasma in both controls (no ALM) and ALM treatment compared to room temperature (p < 0.05); no differences were observed between the ALM and control groups.
Conclusions:
The mechanism of ALM's protective effect remains unclear; key cellular functions may be required to provide protection. In this study, improvements in collagen and thrombin receptor activation peptide aggregation were seen when compared to 4°C-stored plasma samples although no improvements were seen when compared to 4°C-stored platelet additive solution platelets.
Level Of Evidence:
Therapeutic/care management, level II.