Abstract 267 Poster Session III, Monday, 5/3 (poster 111)

CPB is often utilized in infants and children undergoing cardiac surgery. Unfortunately, CPB leads to inflammatory responses that can have deleterious effects on multiple organ systems including the pulmonary system. Current data supports that interventions reducing circulating neutrophils post CPB may improve subsequent pulmonary function and gas exchange. PLV with perfluorocarbons has had application into treatment of pulmonary dysfunction states such as ARDS, with improvements in pulmonary compliance, gas exchange and diminished lung injury when compared to conventional gas ventilation. Recently, we reported that PLV utilized as a lung protection strategy in a neonatal swine model of CPB resulted in increased cardiac output and improved respiratory mechanics. In the present study, we hypothesized that PLV could reduce neutrophil sequestration in the pulmonary parenchyma initiated by CPB, Methods: 22 neonatal piglets (ages 3 to 5 days) were intubated, ventilated, cannulated for bypass, cooled to 18°C after which they underwent low-flow CPB (35 cc/kg/min). After low-flow CPB, animals were rewarmed, taken off CPB and ventilated for 90 min. Of the 22 animals, 8 received conventional ventilation only (control), 7 received initiation of PLV prior to CPB (prevent), and 7 received initiation of PLV during the rewarming phase of CPB (treatment). After 90 min of ventilation, post-CPB, lungs were removed en bloc and the left lobe was dissected the airway identified, and formalin-fixed via the airway at a constant pressure (20 cm H2O) overnight, after which the lungs were paraffin embedded. Neutrophil counting was undertaken using histochemical techniques (leukocyte esterase) and lung injury assessed histologically by the ratio of alveolar wall area to total area in 10 random high-powered fields. Log transformation of the data was undertaken when necessary to equalize the variance between groups. (Table)

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Results: Histological specimens revealed significantly lower number of neutrophils in the lung parenchyma of animals treated with PLV in either the prevent or treatment modes than in the lungs of control animals. There were no differences in histological assessments of lung injury in either group. In conclusion, our findings suggest that PLV is useful in inhibiting the lung inflammatory responses to CPB, and that the effect of the altered lung inflammatory responses on lung injury will need to be studied for longer durations after CPB.

Supported in part by AAP Resident Research Grant