The effects of heparin bound surface modification (Carmeda® Bioactive Surface) on human platelet alterations during simulated extracorporeal circulation

Abstract

To determine if treatment with covalently bound heparin (Carmeda Bioactive Surface (CBAS))a to the synthetic surface of the extracorporeal circuit (ECC) would alter the stereotypic pattern of adverse platelet alterations, 450 ml of heparinized blood (IU/ml) was recirculated at a flow rate of twice the circulating volume (L/min) for 2 hrs at 37°C through either untreated (CONT,n=7) or treated (CBAS,n=7) circuits constructed of identical components including a pediatric (0.8m2) reversed hollow fiber membrane oxygenator. In CONT circuits, platelet count maintained 88+1% (x±SEM) of its initial level in the circuit prime sample, dropped to 36±6% after 5 min, and returned to 56±2% following 2 hrs of ECC. In CBAS circuits, platelet count in the circuit prime sample demonstrated 90±4%, decreased to 68±10% after 5 min (p<0.05) and declined further to 45±5% after 2 hrs (NS). Although platelets from both groups retained reactivity to ADP after priming the circuit, only at 5 min of recirculation did CBAS circuits significantly preserve this responsiveness. In CONT circuits, baseline plasma levels of platelet factor 4 rose from 24±3 to 581±82 ng/ml in the primed circuit and continued to rise to 2933±276 ng/ml by 2 hrs of ECC. In contrast, CBAS circuits markedly reduced this release after 2 hrs (577±165 ng/ml). Furthermore, by 2 hrs of ECC, plasma levels of thromboxane B2 in the CBAS circuits were significantly reduced when compared to CONT circuits (3035±1529 vs 29916±16293 pg/ml, respectively). We conclude that CBAS modification of the simulated extracorporeal circuit preserved the initial circulating platelet count with retained ADP reactivity and markedly decreased release of platelet factor 4 and thromboxane B2.