Heparin-coated bypass circuits reduce pulmonary injury

Abstract

Heparin coating of the extracorporeal circuit not only reduces heparin requirements during cardiac operations but also may reduce organ injury associated with cardiopulmonary bypass (CPB). To examine this possibility, pulmonary injury and neutrophil adhesion molecule expression after CPB were studied in pigs undergoing CPB with a standard extracorporeal circuit (group S, n = 6) or a heparin-coated CPB circuit (Carmeda BioActive Surface) (group HC, n = 6). Pigs received heparin sodium (300 U/kg intravenously) and then underwent 90 minutes of hypothermie (28 °C) CPB using membrane oxygenators, followed by 2 hours of observation. Blood samples were obtained for determination of neutrophil number and expression of the neutrophil adhesion molecule subunit CD18 (by immunofluorescence flow cytometry). The CPB-associated injury was less in group HC. Two hours after CPB, the arterial oxygen tension group was higher in group HC (597.2 ± 31.2 versus 220.5 ± 42.3 mm Hg; p < 0.0001), the pulmonary vascular resistance was lower in these animals (408.6 ± 69.4 versus 1,159.8 ± 202.4 dyne · s · cm −5; p = 0.02), and the static compliance was higher in group HC (66.4 ± 5.4 versus 39.8 ± 5.8 mL/mm Hg; p = 0.004). After 60 minutes of CPB, both groups had similar increases in expression of the neutrophil adhesion molecule subunit CD18 (29.4% ± 19.5% versus 26.0% ± 24.4%, group S and group HC, respectively) and similar decreases in neutrophil counts (6,056 ± 1,285 to 2,453 ± 979 cells/μL versus 6,010 ± 1,748 to 3,197 ± 1,225 cells/μL, group S and group HC, respectively). This study demonstrates that heparin coating improves pulmonary function after CPB and that this effect is not mediated by altered neutrophil kinetics or adhesion molecule expression.