Functional Restoration of Platelets by Tri‐block Polymer (Vepoloaxmer) as Studied in Agonist Induced Platelet Aggregation Studies
Authors: Abro Schuharazad , Guler Nil , Emanuele Marty , Iqbal Omer , Hoppensteadt Debra , Jeske Walter , Emanuele Nicholas , Fareed Jawed 
Published: November 2023

Introduction

Vepoloaxmer (VP) is an amphiphilic, non‐ionic, tri‐block copolymer surfactant. It has been shown to be effective in the repair/recovery of damaged cell membranes. It enhances the survival of red blood cells by increasing the stability of the membrane and decreasing the fragility profile. VP is an attractive and promising agent for enhancing the blood cell viability and functions during prolonged storage in blood banking. Platelets gradually lose their functionality during storage. The aim of the study is to test the protective effect of VP on platelet function.

Material and Methods

Blood samples were collected in 3.2% sodium citrate from 30 heathy volunteers. To investigate the effect of VP on platelet function two experimental methods were used. In the first approach, VP was added to citrated whole blood (WB) in a 1:10 ratio at a final concentration of 10 mg/mL. For control studies, saline was used in the same manner. Saline and VP containing tubes were centrifuged to collect Platelet Rich Plasma (PRP) and platelet poor plasma (PPP). These were referred to ‘saline‐WB‐preparation (saline‐WBP)’ and ‘VP‐WB‐preparation (VP‐WBP)’. In second procedure, citrated WB was centrifuged to obtain PRP and PPP. VP was added to PRP at a concentration of 10 mg/mL. For control purposes, saline was used in the same manner. These were referred to saline‐ PRP‐preparation (saline‐PRPP) and ‘VP‐PRP‐preparation (VP‐PRPP). Similar procedures were repeated at lower concentrations. Agonist induced aggregation (AIA) studies were performed at 30 minutes (min), 180 min and >300minutes at all different concentrations utilizing at PAP‐8 aggregometer (Biodata Corporation). Such agonists as ADP, Arachiconic Acid (AA), Collagen and Epinephrine were used.

Results

In the saline supplemented systems all the agonists showed a time dependent decrease in platelet aggregation induced by different agonists. In the VP supplemented systems there was no protective effect of VP on AA and Epinephrine induced aggregation. However, there was a protective effect on ADP and Collagen induced aggregation except at 10 mg‐WBP. After 300 min, the observed protective effect of on ADP induced aggregation was found to be 40–60% higher in comparison to saline control in 2mg‐WBP. This protective effect was found to be 43 % at 10mg‐PRPP and 10% at 2mg‐PRPP. After 300 min, protective effect on Collagen induced aggregation was 65% compared to saline control in 2mg‐WBP. This protective effect was 42 % at 10mg‐PRPP and 11% at 2mg‐PRPP. The aggregation values were lower in platelets recovered from VP‐WBP in comparison to VP‐PRPP with the exception of epinephrine induced aggregation.

Discussion

Platelets are known to lose their functionality upon storage. In this study, protective effects of VP were observed on ADP and collagen induced aggregation while a decrease aggregation response was noted with AA and Epinephrine aggregation. This suggests that VP modulates specific receptors on platelet surface. Since ADP and Collagen receptors have a major role in aggregation, the protective effects of VP on these receptors may be contributory to the restoration of platelet functionality upon storage.