Abstract

Interleukin-8 (IL-8), the major neutrophil chemoattractant factor, contributes to inflammatory tissue injury by activating neutrophils and promoting their migration into tissue. IL-8 levels increase in serum of patients undergoing cardiopulmonary bypass (CPB). The purpose of this study was to determine if IL-8 gene expression is activated in tissues subjected to CPB with or without hypothermic arrest. IL-8 transcript levels were measured by ribonuclease protection in samples of human atrium and skeletal muscle from children before and after CPB for repair of congenital heart defects. Results were quantified by PhosphorImager. Atrial IL-8 mRNA levels increased during CPB in 14 of 16 patients tested (median increase, 2.9-fold; P = .0029). In skeletal muscle, IL-8 mRNA increased in 11 of 12 patients (median, 12-fold; P = .012). Degree of IL-8 induction in atrium and muscle was not directly associated with total support time or cross-clamp time. Transcript increase in skeletal muscle occurred with or without a period of circulatory arrest, suggesting that the stimulus of CPB alone was sufficient to induce message production. Baseline values for IL-8 mRNA varied widely among patients in atrium and skeletal muscle. In situ hybridization analysis revealed diffuse increase in IL-8 mRNA throughout the tissue after CPB, with striking increase in some small veins. We conclude that production of IL-8 mRNA occurs in most patients during CPB in both myocardium and skeletal muscle. This may result in high local IL-8 concentrations, contributing to the tissue injury after CPB.

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