Abstract
Cardiopulmonary bypass (CPB) is used increasingly to correct cyanotic heart defects during early infancy, but myocardial dysfunction is often seen after surgical repair. This study evaluates whether starting CPB at a conventional, hyperoxic pO2 causes an uninattended reoxygcnalion (RcO2) injury. We subjected 2-week-old pigs to ventilator hypoxemia [FIO2 = 0.06 & pO2 = 25 minHg] followed by 5 min of ReO2 on CPB before instituting cardioplegia. CPB was begun in hypoxemic piglets by either abrupt RcO2 at a pO2 of 400 mmHg [standard clinical practice] or by maintaining a pO2 = 25 mmHg on CPB until controlling ReO2 with blood cardioplegic arrest at a pO2 = 400. Myocardial NO production [chemilumincscence measurements of NO2- + NO3- in aortic and coronary sinus blood] and conjugated diene (CD) generation [spectrophotometric A233 measurements of lipid extracts of blood] were assessed during cardioplegic induction. Thirty min after CPB, left ventricular end-systolic clastance [Ees, catheter conductance method] was used to determine cardiac function. CPB and blood cardioplegic arrest caused no functional or biochemical change in normoxic (control) versus hypoxemic hearts. Abrupt RcO2 caused a 10-fold rise in NO and CD production by the heart with subsequent depression of myocardial function (Ecs = 21 ±2% of control). In contrast, controlled cardiac ReO2 reduced NO production by 50%, CD did not rise, and Ecs was 83±8% of normal. We conclude controlled ReO2 when starting CPB to correct cyanotic heart defects may improve myocardial status post-operatively.
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Sherman, M., Buckberg, G., Monta, K. et al. CONTROLLED CARDIAC REOXYGENATION REDUCES NITRIC OXIDE (NO) PRODUCTION AND OXIDANT INJURY OP HYPOXEMIC INFANT HEARTS. Pediatr Res 35, 260 (1994). https://doi.org/10.1203/00006450-199402000-00033
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DOI: https://doi.org/10.1203/00006450-199402000-00033