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Effects of cardiopulmonary bypass on eicosanoid metabolism during pediatric cardiovascular surgery
W J Greeley1, G A Bushman, D L Kong
1Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710.
Insights
Pediatric cardiopulmonary bypass significantly alters eicosanoid production, increasing thromboxane levels, especially in younger children. However, thromboxane does not appear to directly cause pulmonary hypertension or platelet loss during these operations.
Area of Science:
- Biochemistry
- Pediatric Cardiology
- Vascular Biology
Background:
- Cardiopulmonary bypass (CPB) in children with congenital heart disease causes morbidity, including coagulopathy and pulmonary vascular changes.
- Prostaglandins (eicosanoids) are implicated in the adult response to extracorporeal circulation.
Purpose of the Study:
- To assess the effect of CPB on thromboxane and prostacyclin levels in pediatric patients.
- To evaluate the relationship between eicosanoid changes and platelet loss or pulmonary hemodynamics during CPB.
Main Methods:
- Measured thromboxane and prostacyclin concentrations in 21 children undergoing CPB for congenital heart defects.
- Compared these levels with 9 pediatric control patients without CPB.
- Correlated eicosanoid levels with platelet counts and pulmonary vascular resistance.
Main Results:
- Thromboxane levels significantly increased during CPB (p < 0.005), with higher levels in younger children (p < 0.002).
- Prostacyclin levels increased in both CPB and control groups, likely due to surgical manipulation.
- No significant correlation found between thromboxane changes and pulmonary vascular resistance, platelet loss, or CPB duration.
Conclusions:
- Eicosanoid production is significantly altered in children during CPB.
- Increased thromboxane during CPB does not directly mediate pulmonary hypertension or platelet loss in pediatric cardiovascular surgery.
Abstract:
Cardiopulmonary bypass in children with congenital heart disease is associated with significant morbidity manifested by increased complement degradation products, heightened pulmonary vascular activity, and coagulopathy. In adults with cardiac disease, the prostaglandins (eicosanoids) have been shown to contribute to the pathophysiologic response to extracorporeal circulation. This study assessed the effect of cardiopulmonary bypass in infants and children on two potent eicosanoids: thromboxane, a vasoconstrictor and platelet aggregating agent, and prostacyclin, a vasodilator and platelet disaggregating agent. The biochemical profiles of thromboxane and prostacyclin were evaluated in temporal relationship to selected parameters of platelet loss and pulmonary vascular hemodynamics during and after cardiopulmonary bypass. Twenty-one children, aged 3 days to 9 years, with congenital heart defects who were undergoing repair with cardiopulmonary bypass were studied. Nine pediatric patients undergoing palliative heart operations with no cardiopulmonary bypass served as the control group. In the group having cardiopulmonary bypass, the thromboxane concentration significantly increased during bypass (195 +/- 10 to 910 +/- 240 pg/ml, +/- standard error of the mean, p less than 0.005), whereas the control group demonstrated no significant change in thromboxane concentration. The highest thromboxane values were seen in the youngest patients (p less than 0.002). There was no significant correlation between thromboxane changes with alterations in pulmonary vascular resistance, platelet loss, duration of cardiopulmonary bypass or aortic cross-clamping. Prostacyclin levels rose significantly in both the bypass group (100 +/- 20 to 570 +/- 80 pg/ml, p less than 0.01) and in the control group (109 +/- 44 to 589 +/- 222 pg/ml, p less than 0.01), which apparently is due to surgical manipulation of vascular endothelium. These data show that eicosanoid production is significantly altered in children during cardiopulmonary bypass. Although thromboxane, a potent vasoconstrictor, is produced in significant amounts during and after cardiopulmonary bypass, our data show that thromboxane does not directly mediate changes in pulmonary artery hypertension and is not quantitatively related to platelet loss during pediatric cardiovascular operations.