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Interleukin-8 release and neutrophil degranulation after pediatric cardiopulmonary bypass
1Division of Cell and Molecular Biology, Institute of Child Health, London, England.
Insights
Pediatric cardiopulmonary bypass surgery significantly increases circulating interleukin-8 levels, linked to neutrophil activation and capillary leak. This cytokine release is a key factor in post-cardiac surgery complications.
Area of Science:
- Pediatric Cardiology
- Immunology
- Surgical Complications
Background:
- Capillary leak syndrome is a serious complication in children undergoing cardiopulmonary bypass for congenital heart defects.
- Neutrophil-mediated endothelial injury is a suspected cause of this capillary leak.
Purpose of the Study:
- To investigate the activation pathways of neutrophils during and after cardiopulmonary bypass.
- To examine the role of interleukin-8 in pediatric cardiopulmonary bypass-associated capillary leak.
Main Methods:
- A prospective controlled descriptive study involving 18 children (9 cardiac surgery with bypass, 9 neurosurgery without bypass).
- Arterial blood samples were collected at multiple time points before, during, and after surgery.
- Circulating levels of interleukin-8, interleukin-1 alpha, interleukin-1 beta, tumor necrosis factor-alpha, elastase alpha 1-antitrypsin, and neutrophil counts were measured.
Main Results:
- Six of nine cardiac patients showed a significant rise in circulating interleukin-8 (IL-8) starting during rewarming and peaking post-bypass.
- IL-8 release strongly correlated with bypass duration, elastase alpha 1-antitrypsin levels, and absolute neutrophil counts in cardiac patients.
- Only one neurosurgery patient exhibited elevated IL-8, indicating a specific link to cardiopulmonary bypass.
Conclusions:
- Pediatric hypothermic cardiopulmonary bypass triggers the release of interleukin-8 into circulation.
- Elevated IL-8 levels, associated with neutrophil degranulation, likely contribute to the pathophysiology of capillary leak after cardiac surgery.
- This finding supports IL-8 as a critical mediator in post-cardiac surgery complications.
Abstract:
Capillary leak after cardiopulmonary bypass operations for correction of congenital heart defects is universally seen in children and often causes significant morbidity and mortality. Since neutrophil-mediated endothelial injury has been implicated as a pathogenetic mechanism, a prospective controlled descriptive study was performed to investigate possible activation pathways during and after the bypass procedure. Eighteen children undergoing operations, nine with cardiopulmonary bypass and nine neurosurgical craniotomy (i.e., operations without bypass), had samples of arterial blood collected at intervals before, during, and after operations. In six of nine cardiac patients circulating interleukin-8 concentrations rose from less than 30 pg/ml to very high concentrations (> 500 pg/ml); in the remaining three patients small rises (peak 57 to 81 pg/ml) were also seen. In all nine, the rise commenced at the time of rewarming, toward the end of bypass, and peaked 1 to 3 hours thereafter. Interleukin-8 release correlated significantly with length of bypass. Interleukin-1 alpha and interleukin-1 beta were not found, and traces of tumor necrosis factor-alpha were detected in one patient only. Circulating elastase alpha 1-antitrypsin concentrations rose simultaneously and correlated significantly with interleukin-8 (p < 0.001) in patients with cardiac disease, as did absolute neutrophil counts (p < 0.001). In contrast, only one of nine patients with neurosurgical disease (undergoing an unusually long operation and exchange transfusion) had a rise in circulating interleukin-8 to levels greater than 500 pg/ml (p < 0.01). The two samples from this patient with elevated interleukin-8 were the only neurosurgical samples with elevated elastase. This study demonstrates the release of interleukin-8 into the circulation after pediatric hypothermic cardiopulmonary bypass and supports the suggestion that this cytokine plays a role in the pathophysiology of capillary leak through neutrophil degranulation.