(Circulation. 2000;101:541.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
From the Departments of Surgery (P.J.C., D.M.C., G.Q., J.J., R.M.U.) and Pediatrics, Division of Pediatric Cardiology (R.N., A.E.O., S.P.S., P.A.W.A.), Duke University, Durham, NC.
Correspondence to Page A.W. Anderson, MD, DUMC, Box 3218, Durham, NC 27710. E-mail ander005{at}mc.duke.edu
BackgroundHost 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 ResultsTwenty 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 (
), 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±3.2x103 vs n=6, 34.3±3.7x103
erg/cm3, P=0.042);
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).
ConclusionssCR1 meaningfully moderates the post-CPB syndrome, supporting the hypothesis that complement activation contributes to this syndrome.
Key Words: cardiopulmonary bypass diastole myofilaments calcium
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