Perflubron emulsion reduces inflammation during extracorporeal circulation

The recovery from cardiac surgery and cardiopulmonary bypass can be complic ated by an acute inflammatory response. Circulating blood through an extrac orporeal circuit (ECC) contributes to this complication. Perfluorocarbon-ba sed blood substitutes (PFCs) are under investigation for use as a component of the ECC "prime" solution, because PFCs increase the oxygen-carrying cap acity of the diluted blood. Some PFCs may provide the additional benefit of attenuating the ECC-induced inflammatory response. Earlier, we reported th at perflubron emulsion (PFE, Alliance Pharmaceutical Corp.) reduced neutrop hil (PMN) activation in vivo. However, the potential of PFE to reduce ECC-i nduced PMN activation has not been investigated. In this study, we used a s mall-scale ECC model to quantify the extent of PMN activation during circul ation and to examine if PFE treatment attenuated PMN activation. ECC circui ts were filled with a mixture of blood and Plasmalyte. Two groups were stud ied: an untreated group containing blood plus PlasmaLyte and a treated grou p in which some of the Plasmalyte was substituted with PFE (4.5 g/100 mi). Hematology and measures of whole blood PMN activation were made from blood samples taken periodically throughout the 120-min ECC circulation period. W e found, for the untreated group, a significant decrease in the number of c irculating PMNs and an increase in PMN activation with time. PMN activation was demonstrated as a significant increase in the expression of the PMN ad hesion protein CD11b (P < 0.05) and an increase in PMN oxygen free radical production (reactive oxygen species (ROS)). After 120 min of circulation, t he PMNs remained capable of a significant response to a second inflammatory stimulus, but PFE treatment significantly attenuated the fMLP-induced incr ease in PMN ROS at t = 120 min (P < 0.05). These results suggest that PFE m ay have dual utility in cardiac surgery, to increase oxygen delivery and to serve as an antiinflammatory agent. (C) 2001 Academic Press.