Soluble complement receptor-1 protects heart, lung, and cardiac myofilament function from cardiopulmonary bypass damage

Background-Host defense system activation occurs with cardiopulmonary bypas s (CPB) and is thought to contribute to the pathophysiological consequences of CPB. Complement inhibition effects on the post-CPB syndrome were tested with soluble complement receptor-1 (sCR1). Methods and Results-Twenty neonatal pigs (weight 1.8 to 2.8 kg) were random ized to control and sCR1-treated groups. LV pressure and volume, left atria l pressure, pulmonary artery pressure and flow, and respiratory system comp liance and resistance were measured. Preload recruitable stroke work, isovo lumic diastolic relaxation time constant (tau), and pulmonary vascular resi stance were determined. Pre-CPB measures were not statistically significant ly different between the 2 groups. After CPB, preload recruitable stroke wo rk was significantly higher in the sCR1 group (n=5, 46.8+/-3.2X10(3) vs n=6 , 34.3+/-3.7x10(3) erg/cm(3), P=0.04 2); tau was significantly lower in the sCR1 group (26.4+/-1.5, 42.4+/-6.6 ms, P=0.003); pulmonary vascular resist ance was significantly lower in the sCR1 group (5860+/-1360 vs 12170+/-1200 dyn.s/cm(5), P=0.009); arterial PO2 in 100% FiO(2) was significantly highe r in the sCR1 group (406+/-63 vs 148+/-33 mm Hg, P=0.01); lung compliance a nd airway resistance did not differ significantly. The post-CPB Hill coeffi cient of atrial myocardium was higher in the sCR1 group (2.88+/-0.29 vs 1.8 8+/-0.16, P=0.023). Conclusions-sCR1 meaningfully moderates the post-CPB syndrome, supporting t he hypothesis that complement activation contributes to this syndrome.