953-35 Reduction of Nitric Oxide Induced Reoxygenation Injury in the Cyanotic Immature Heart by Controlling Oxygen Content

Abstract

Abrupt reoxygenation of cyanotic infants on cardiopulmonary bypass (CPB) is followed by a burst of nitric oxide (NO). and oxygen free radicals, leading to impaired myocardial contractility. This oxygen related damage may be reduced by controlling pO 2 during initial reoxygenation. Twenty-five piglets (2–3 weeks) were made hypoxic on Ventilator for 2 hours. Six were not made hypoxic (Control) . Simulating clinical routine, 9 hypoxic piglets were placed on hyperoxic (pO 2 400 mmHg) CPS (Hyperoxic) . Five others were put on normoxic (pO 2 100 mmHg) (Normoxic) , and 5 underwent hypoxic CPS at ambient pO 2 (25 mmHg). delaying reoxygenation until blood cardioplegic (BCP) arrest (Hypoxic). During 30 a min period of SCP-arrest Nitric oxide (pmol/100 g/min) and conjugated diene production (A 233 nm/100 g/min) were measured. Post CPB measurements included % recovery of end-systolic elastance (impedance catheter), and tissue antioxidant reserve capacity (MDA production after exposure to t-BOOH). Ensystolic elastance Anti oxidant reserve capacity Conjugated Diene production Nitric Oxide production Control 102 ± 7 943 ± 88 3.2 ± 1 270 ± 182 Hyperoxic 21 ± 2 # 1342 ± 89 # 420 ± 4.4 # 4767 ± 2455 # Normoxic 56 ± 11 * 939 ± 74 * 15.5 ± 3.1 * 1264 ± 736 * Hypoxic 83 ± 8 * 982 ± 88 * 1.8 ± l.4 * , † 309 ± 88 * , † # P < 0.05 vs. Control. * p < 0.05 vs. Hyperoxic, † = P< 0.05 vs. Normoxic These data document a NO and oxygen free radical related injuryin the hypoxic immature heart after hyperoxic reoxygenation on CPS Inormal clinical routine). Controlling pO 2 during the initial reoxygenation period resulted in dose dependent less NO production, and in improved biochemical and functional status. Clinical application of “controlled reoxygenation” could improve myocardial protection in cyanotic immature hearts on CPB and improve clinical outcome.