Background—Host defense system activation occurs with cardiopulmonary bypass (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 randomized to control and sCR1-treated groups. LV pressure and volume, left atrial pressure, pulmonary artery pressure and flow, and respiratory system compliance and resistance were measured. Preload recruitable stroke work, isovolumic diastolic relaxation time constant (τ), and pulmonary vascular resistance were determined. Pre-CPB measures were not statistically significantly different between the 2 groups. After CPB, preload recruitable stroke work was significantly higher in the sCR1 group (n=5, 46.8±3.2×10³ vs n=6, 34.3±3.7×10³ erg/cm³, P=0.042); τ was significantly lower in the sCR1 group (26.4±1.5, 42.4±6.6 ms, P=0.003); pulmonary vascular resistance was significantly lower in the sCR1 group (5860±1360 vs 12 170±1200 dyn · s/cm⁵, P=0.009); arterial Po₂ in 100% Fio₂ was significantly higher in the sCR1 group (406±63 vs 148±33 mm Hg, P=0.01); lung compliance and airway resistance did not differ significantly. The post-CPB Hill coefficient of atrial myocardium was higher in the sCR1 group (2.88±0.29 vs 1.88±0.16, P=0.023).

Conclusions—sCR1 meaningfully moderates the post-CPB syndrome, supporting the hypothesis that complement activation contributes to this syndrome.