Neutrophil degranulation and complement activation during fetal cardiac bypass

Background. Fetal cardiac bypass results in dysfunction of the fetoplacenta l unit (FPU) characterized by increased placental vascular resistance and r espiratory acidosis. However the mechanisms of this dysfunction are not com pletely understood. To test the hypothesis that complement activation and n eutrophil degranulation may contribute to the placental dysfunction associa ted with fetal bypass, we compared placental hemodynamics, complement activ ation, and neutrophil degranulation among fetuses exposed to cardiac bypass with a miniaturized bypass circuit including an in-line axial flow pump (H emopump), fetuses undergoing bypass with a conventional roller pump circuit , and control fetuses that were similarly exposed but did not undergo bypas s. Methods. Twenty-six Western Cross sheep fetuses (median 122 days gestation) were randomly assigned to undergo cardiac bypass for 30 minutes with the H emopump circuit (n = 8), to undergo bypass for 30 minutes with the conventi onal (roller pump) circuit (n = 10), or to undergo identical exposure and c annulation but not bypass (n = 8, controls). Blood samples were collected t o measure white cell count and differential, and C3a and lactoferrin levels prior to bypass, at the end of bypass, and 1 and 2 hours after bypass. Hem odynamics and blood gases were also monitored. Results. There was a fall in white cell count over time that continued afte r bypass in all groups; neutrophils and lymphocytes were affected similarly . C3a levels rose significantly from prebypass to postbypass in the roller pump group (p < 0.0001) but not in either of: the other groups. Lactoferrin levels rose significantly from start of bypass in both bypass groups (Hemo pump p = 0.01; roller pump p < 0.0001) but not in controls. The elevation i n lactoferrin level coincided with worsening placental gas exchange and det eriorating cardiac function. Conclusions. Complement and neutrophil activation occurred with fetal cardi ac bypass but only neutrophil activation mirrored the FPU and cardiac dysfu nction, suggesting that products of neutrophil activation may be important contributing factors. Improved FPU function with a bypass circuit that has less extracorporeal surface and does not require a large priming volume may be due in part to a reduction in the magnitude of this inflammatory respon se. (C) 2000 by The Society of Thoracic Surgeons.