OBJECTIVE: Cardiopulmonary bypass induces a systemic inflammatory response that causes substantial clinical morbidity. This study sought to determine cellular and humoral variables of inflammation. We hypothesized that chemokines are a major source of stimulation of neutrophils and monocytes in pediatric cardiac surgery. METHODS: We performed an observational prospective clinical study of 20 pediatric patients before and after cardiopulmonary bypass. Plasma levels of interleukin-6, interleukin-8, myeloperoxidase, and nitric oxide were measured by immunoassays. Expression of interleukin-8 receptors (CXCR1, CXCR2) and CD14 of circulating neutrophils and monocytes was assessed by flow cytometry. Clinical evaluations included length of inotropic support and mechanical ventilation as well as oxygenation. RESULTS: Two hours after cardiopulmonary bypass, plasma levels of interleukin-6 and interleukin-8 were strongly increased (P =.0001 and P =.0032, respectively). Interleukin-6 and interleukin-8 concentrations correlated with the length of inotropic support, as well as with the length of mechanical ventilation (r >.70, P </=.0006), and were inversely related to the ratio of arterial oxygen tension to fraction of inspired oxygen. There was a strong association between the postoperative levels of interleukin-6 and nitric oxide, as well as between interleukin-6 and CD14 expression on monocytes (r >.62, P </=.0031). The expression of CXCR2 but not CXCR1 on neutrophils and monocytes correlated negatively with the levels of interleukin-8 and myeloperoxidase. CONCLUSIONS: After cardiopulmonary bypass, impairment of cardiovascular and respiratory function correlated with the levels of interleukin-6 and interleukin-8 as mediators of an inflammatory response. The negative correlation of CXCR2 expression with interleukin-8 and myeloperoxidase indicates that myeloid cells were stimulated by CXC chemokines with Glu-Leu-Arg (ELR) motif and thereby contributed to tissue damage, leading to impairment of cardiovascular and respiratory function.
OBJECTIVE: Cardiopulmonary bypass induces a systemic inflammatory response that causes substantial clinical morbidity. This study sought to determine cellular and humoral variables of inflammation. We hypothesized that chemokines are a major source of stimulation of neutrophils and monocytes in pediatric cardiac surgery. METHODS: We performed an observational prospective clinical study of 20 pediatric patients before and after cardiopulmonary bypass. Plasma levels of interleukin-6, interleukin-8, myeloperoxidase, and nitric oxide were measured by immunoassays. Expression of interleukin-8 receptors (CXCR1, CXCR2) and CD14 of circulating neutrophils and monocytes was assessed by flow cytometry. Clinical evaluations included length of inotropic support and mechanical ventilation as well as oxygenation. RESULTS: Two hours after cardiopulmonary bypass, plasma levels of interleukin-6 and interleukin-8 were strongly increased (P =.0001 and P =.0032, respectively). Interleukin-6 and interleukin-8 concentrations correlated with the length of inotropic support, as well as with the length of mechanical ventilation (r >.70, P </=.0006), and were inversely related to the ratio of arterial oxygen tension to fraction of inspired oxygen. There was a strong association between the postoperative levels of interleukin-6 and nitric oxide, as well as between interleukin-6 and CD14 expression on monocytes (r >.62, P </=.0031). The expression of CXCR2 but not CXCR1 on neutrophils and monocytes correlated negatively with the levels of interleukin-8 and myeloperoxidase. CONCLUSIONS: After cardiopulmonary bypass, impairment of cardiovascular and respiratory function correlated with the levels of interleukin-6 and interleukin-8 as mediators of an inflammatory response. The negative correlation of CXCR2 expression with interleukin-8 and myeloperoxidase indicates that myeloid cells were stimulated by CXC chemokines with Glu-Leu-Arg (ELR) motif and thereby contributed to tissue damage, leading to impairment of cardiovascular and respiratory function.
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