We tested the hypothesis that administering polyethylene glycol-conjug
ated superoxide dismutase (PEG-SOD) either before global cerebral isch
emia or at the time of reperfusion would alter recovery of cerebral bl
ood flow (CBF; microspheres) response to alteration in arterial PCO2 i
n pentobarbital-anesthetized, mechanically ventilated piglets (1 to 2-
wk old). CBF was measured at an arterial PCO2 of approximately 3.3, 5.
3, and 8.7 kPa before and 2 h after ischemia (10 min aortic cross clam
p). To determine the effect of preischemic versus postischemic treatme
nt with PEG-SOD, each piglet received two i.v. drug injections of eith
er 30 000 U PEG-SOD or an equal volume of PEG diluent in a randomized,
blinded fashion before ischemia and just before reperfusion. Cerebral
oxygen consumption and somatosensory evoked potentials were measured
during reperfusion as an assessment of brain function. During reperfus
ion, no group demonstrated delayed hypoperfusion. Hypercapnic CBF was
less during reperfusion (48 t 6 mL/min/100 g)compared with preischemia
(69 +/- 10 mL/min/100 g) in PEG/PEG-treated piglets. However, hyperca
pnic CBF during reperfusion was not different from preischemic values
with either preischemic or postischemic PEG-SOD treatment. Improved re
turn of hypercapnic CBF in PEG-SOD-treated piglets was not attributabl
e to improved postischemic cerebral oxygen consumption. Somatosensory
evoked potential amplitude was decreased similarly during reperfusion
(approximately 25% of preischemic values) in all groups. We conclude t
hat PEG-SOD alters CBF response to hypercapnia after transient global
cerebral ischemia in piglets via a mechanism that is not related to al
tered oxygen consumption or electrical activity.