TY - JOUR
T1 - Superoxide dismutase and catalase do not affect the pulmonary hypertensive response to group B streptococcus in the lamb
AU - Carpenter, D. T.
AU - Larkin, H. R.
AU - Chang, A. S.
AU - Morris, E.
AU - O'Neill, J. T.
AU - Curtis, J.
PY - 2001
Y1 - 2001
N2 - 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 Pao2 was maintained > 100 mm Hg. The control group received saline vehicle only (n = 6), the GBS group received GBS infusion only (n = 9), the enzymes (ENZ) group received polyethylene glycol-superoxide dismutase (PEG-SOD) and polyethylene glycol-catalase (PEG-CAT) treatment only (n = 6), and the ENZ+GBS group received PEG-SOD and PEG-CAT then GBS (n = 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 ENZ+GBS groups, respectively. Sixty minutes after the termination of the GBS infusion, PVR returned to baseline in the GBS group but did not in the ENZ+GBS 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.
AB - 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 Pao2 was maintained > 100 mm Hg. The control group received saline vehicle only (n = 6), the GBS group received GBS infusion only (n = 9), the enzymes (ENZ) group received polyethylene glycol-superoxide dismutase (PEG-SOD) and polyethylene glycol-catalase (PEG-CAT) treatment only (n = 6), and the ENZ+GBS group received PEG-SOD and PEG-CAT then GBS (n = 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 ENZ+GBS groups, respectively. Sixty minutes after the termination of the GBS infusion, PVR returned to baseline in the GBS group but did not in the ENZ+GBS 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.
UR - http://www.scopus.com/inward/record.url?scp=0035144329&partnerID=8YFLogxK
U2 - 10.1203/00006450-200102000-00009
DO - 10.1203/00006450-200102000-00009
M3 - Article
C2 - 11158511
AN - SCOPUS:0035144329
SN - 0031-3998
VL - 49
SP - 181
EP - 188
JO - Pediatric Research
JF - Pediatric Research
IS - 2
ER -