期刊
PEDIATRIC CARDIOLOGY
卷 33, 期 4, 页码 562-568出版社
SPRINGER
DOI: 10.1007/s00246-012-0166-2
关键词
Cardiopulmonary bypass; Congenital heart disease; Isoprostanes; Oxidative stress
资金
- NIH [NS050396, GM07569-32]
- NCRR/NIH (Vanderbilt Institute for Clinical and Translational Research) [1 UL1 RR024975]
- [P30HD15052]
Cardiopulmonary bypass (CPB) produces inflammation and oxidative stress, which contribute to postoperative complications after cardiac surgery. F-2-Isoprostanes (F-2-IsoPs) are products of lipid oxidative injury and represent the most accurate markers of oxidative stress. In adults undergoing cardiac surgery, CPB is associated with elevated IsoPs. The relationship between F-2-IsoPs and perioperative end-organ function in infants with single-ventricle physiology, however, has not been well studied. This study prospectively enrolled 20 infants (ages 3-12 months) with univentricular physiology undergoing elective stage 2 palliation (bidirectional cavopulmonary anastomosis). Blood samples were collected before the surgical incision (T0), 30 min after initiation of CPB (T1), immediately after separation from CPB (T2), and 24 h postoperatively (T3). Plasma F-2-IsoP levels were measured at each time point and correlated with indices of pulmonary function and other relevant clinical variables. Plasma F-2-IsoPs increased significantly during surgery, with highest levels seen immediately after separation from CPB (p < 0.001). After separation from CPB, increased F-2-IsoP was associated with lower arterial pH (rho = -0.564; p = 0.012), higher partial pressure of carbon dioxide (PaCO2; rho = 0.633; p = 0.004), and decreased lung compliance (rho = -0.783; p a parts per thousand currency sign 0.001). After CPB, F-2-IsoPs did not correlate with duration of CPB, arterial lactate, or immediate postoperative outcomes. In infants with single-ventricle physiology, CPB produces oxidative stress, as quantified by elevated F-2-IsoP levels. Increased F-2-IsoP levels correlated with impaired ventilation in the postoperative period. The extent to which F-2-IsoPs and other bioactive products of lipid oxidative injury might predict or contribute to organ-specific stress warrants further investigation.
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