HEPARIN-COATED BYPASS CIRCUITS REDUCE PULMONARY INJURY

Heparin coating of the extracorporeal circuit not only reduces heparin requirements during cardiac operations but also may reduce organ inju ry associated with cardiopulmonary bypass (CPB). To examine this possi bility, pulmonary injury and neutrophil adhesion molecule expression a fter CPB were studied in pigs undergoing CPB with a standard extracorp oreal circuit (group S, n = 6) or a heparin-coated CPB circuit (Carmed a BioActive Surface) (group HC, n = 6). Pigs received heparin sodium ( 300 U/kg intravenously) and then underwent 90 minutes of hypothermic ( 28-degrees-C) CPB using membrane oxygenators, followed by 2 hours of o bservation. Blood samples were obtained for determination of neutrophi l number and expression of the neutrophil adhesion molecule subunit CD 18 (by immunofluorescence flow cytometry). The CPB-associated injury w as 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 anim als (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 vers us 39.8 +/- 5.8 mL/mm Hg; p = 0.004). After 60 minutes of CPB, both gr oups had similar increases in expression of the neutrophil adhesion mo lecule subunit CD18 (29.4% +/- 19.5% versus 26.0% +/- 24.4%, group S a nd group HC, respectively) and similar decreases in neutrophil counts (6,056 +/- 1,285 to 2,453 +/- 979 cells/muL versus 6,010 +/- 1,748 to 3,197 +/- 1,225 cells/muL, group S and group HC, respectively). This s tudy demonstrates that heparin coating improves pulmonary function aft er CPB and that this effect is not mediated by altered neutrophil kine tics or adhesion molecule expression.