The purpose of this study was to determine whether treatment with conjugated antioxidant enzymes could attenuate or abolish pulmonary hypertension induced by group B streptococcus (GBS). Lambs, 3-7 d old, were anesthetized and ventilated. Intravascular catheters were placed in the left ventricle, descending aorta, right atrium, and pulmonary artery for continuous monitoring of intravascular pressures. Cardiac output was measured with radiolabeled microspheres. Measurements were obtained at baseline and 15 and 60 min into a 60-min GBS infusion, and 60 min after GBS was stopped. Blood gas values were held constant and Pao 2 was maintained Ͼ100 mm Hg. The control group received saline vehicle only (n ϭ 6), the GBS group received GBS infusion only (n ϭ 9), the enzymes (ENZ) group received polyethylene glycol-superoxide dismutase (PEG-SOD) and polyethylene glycol-catalase (PEG-CAT) treatment only (n ϭ 6), and the ENZϩGBS group received PEG-SOD and PEG-CAT then GBS (n ϭ 9). Plasma samples were obtained to confirm increased superoxide dismutase and catalase activities in the groups receiving enzymes. Compared with baseline, pulmonary vascular resistance increased by 119% and 101% at 15 min and 87% and 81% at 60 min in the GBS and ENZϩGBS groups, respectively. Sixty minutes after the termination of the GBS infusion, PVR returned to baseline in the GBS group but did not in the ENZϩGBS group. Enzyme infusions resulted in at least a ninefold increase in plasma enzyme activities. As opposed to previously published data from endotoxin models, PEG-CAT and PEG-SOD were ineffective in altering the GBS-induced pulmonary hypertensive response in this model. This suggests that acute administration of antioxidant enzymes may not be effective in ameliorating GBS-induced pulmonary hypertension. Morbidity and mortality remain unacceptably high in newborn infants infected with GBS despite aggressive use of antibiotics, both intrapartum and immediately following delivery (1). Many infants infected with this organism develop pulmonary hypertension (2), even in the face of blood cultures that have quickly become sterile. In many of these infants, the high morbidity and mortality is a result of the pulmonary hypertension. There are no unique or specific
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