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   <subfield code="a">Reduction of reoxygenation injury and nitric oxide production in the cyanotic immature heart by controlling pO2</subfield>
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   <subfield code="a">Reintroduction of high levels of molecular oxygen after a hypoxic periodis followed by a burst of nitric oxide (NO), peroxynitrite, and oxygen freeradicals, which are highly cytotoxic. This study tests the hypotheses thata) controlled reoxygenation of cyanotic immature hearts when startingcardiopulmonary bypass (CPB) with high pO2 pressure of oxygen produces areoxygenation injury, and b) this oxygen-related damage is avoidable bycontrolling the circumstances of the reoxygenation period (controlledreoxygenation). Of 40 immature piglets (2-3 weeks), 5 normoxic instrumentedpiglets served as control, and 6 underwent 1 h of CPB including 30 min ofaortic clamping with blood cardioplegic (BCP) arrest without precedinghypoxia (BCP control). Twenty-nine others were made hypoxic (arterial pO220-30 mmHg) for up to 2 h by lowering the forced inspiratory oxygen (FiO2)on a ventilator. They were then reoxygenated on CPB as follows, 1) abruptreoxygenation at pO2 400 mmHg in 5, (Reox), 2) gradual increase in pO2 from30 to 400 mmHg in 5 (Graded Reox), both without BCP arrest, 3) starting CPBat different pO2 levels (hyperoxic, normoxic or hypoxic) for 5 min,followed by BCP arrest (Reox+BCP: pO2 &gt; 400, 100 or 20-30 mmHg), in 19others. Reoxygenation on CPB at pO2 more than 400 mmHg depressedcontractility (endsystolic elastance [Ees] to 25 +/- 5% of control; P &lt;0.05), accompanied by reduced antioxidant reserve capacity [AORC] (P &lt;0.05 vs control), which was only slightly improved by Graded Reox (Ees 34+/- 4%, P &lt; 0.05 vs control).(ABSTRACT TRUNCATED AT 250 WORDS)</subfield>
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