K Ihnken1, K Morita, G D Buckberg. 1. Division of Cardiothoracic Surgery, University of California, Los Angeles, School of Medicine, USA.
Abstract
BACKGROUND: Hypoxemic developing hearts are susceptible to oxygen-mediated damage that occurs after reintroduction of molecular oxygen. This unintended hypoxemic/reoxygenation injury leads to lipid peroxidation and membrane damage and may contribute to postoperative cardiac dysfunction. Biochemical and functional status are improved by delaying reoxygenation on cardiopulmonary bypass (CPB) until cardioplegic arrest. METHODS: Six immature piglets (3 to 5 kg) without hypoxemia underwent 30 minutes of cardioplegic arrest during 1 hour of CPB. Fourteen others underwent 2 hours of hypoxemia on ventilator before reoxygenation on CPB. Reflecting our clinical routine, 9 were reoxygenated on CPB for 5 minutes followed by 30 minutes of cardioplegic arrest and 25 minutes of reperfusion. The other 5 were put on hypoxemic CPB for 5 minutes, before being reoxygenated during cardioplegic arrest for 30 minutes followed by 25 minutes of reperfusion. RESULTS: Cardioplegic arrest (no hypoxemia group) caused no functional or biochemical changes. In contrast, by preceding hypoxemia with subsequent reoxygenation on CPB (no treatment group) we found 39.5% decrease in antioxidant reserve capacity, 1,212% increase in myocardial conjugated diene production, significant increase in coronary sinus blood conjugated dienes, and an 81% reduction of left ventricular contractility, all of which were statistically significant (p < 0.05) when compared with the no hypoxemia group. Conversely, delaying reoxygenation until cardioplegic arrest (treatment group) resulted in 33.1% improvement in antioxidant reserve capacity, 91.7% less conjugated diene production, lower coronary sinus blood conjugated diene levels, and a 95% improved contractility, all of which were significant (p < 0.05) when compared with the no treatment group. CONCLUSIONS: A reoxygenation injury associated with lipid peroxidation and decreased postbypass contractility occurs in cyanotic immature hearts when reoxygenated on CPB. Delaying reoxygenation until cardioplegic arrest by starting CPB with ambient partial pressure of oxygen results in significantly improved myocardial status.
BACKGROUND: Hypoxemic developing hearts are susceptible to oxygen-mediated damage that occurs after reintroduction of molecular oxygen. This unintended hypoxemic/reoxygenation injury leads to lipid peroxidation and membrane damage and may contribute to postoperative cardiac dysfunction. Biochemical and functional status are improved by delaying reoxygenation on cardiopulmonary bypass (CPB) until cardioplegic arrest. METHODS: Six immature piglets (3 to 5 kg) without hypoxemia underwent 30 minutes of cardioplegic arrest during 1 hour of CPB. Fourteen others underwent 2 hours of hypoxemia on ventilator before reoxygenation on CPB. Reflecting our clinical routine, 9 were reoxygenated on CPB for 5 minutes followed by 30 minutes of cardioplegic arrest and 25 minutes of reperfusion. The other 5 were put on hypoxemic CPB for 5 minutes, before being reoxygenated during cardioplegic arrest for 30 minutes followed by 25 minutes of reperfusion. RESULTS:Cardioplegic arrest (no hypoxemia group) caused no functional or biochemical changes. In contrast, by preceding hypoxemia with subsequent reoxygenation on CPB (no treatment group) we found 39.5% decrease in antioxidant reserve capacity, 1,212% increase in myocardial conjugated diene production, significant increase in coronary sinus blood conjugated dienes, and an 81% reduction of left ventricular contractility, all of which were statistically significant (p < 0.05) when compared with the no hypoxemia group. Conversely, delaying reoxygenation until cardioplegic arrest (treatment group) resulted in 33.1% improvement in antioxidant reserve capacity, 91.7% less conjugated diene production, lower coronary sinus blood conjugated diene levels, and a 95% improved contractility, all of which were significant (p < 0.05) when compared with the no treatment group. CONCLUSIONS: A reoxygenation injury associated with lipid peroxidation and decreased postbypass contractility occurs in cyanotic immature hearts when reoxygenated on CPB. Delaying reoxygenation until cardioplegic arrest by starting CPB with ambient partial pressure of oxygen results in significantly improved myocardial status.