Abstract
Purpose
Cardiopulmonary bypass (CPB) is characterized by translocation of intestinal endotoxin and subsequent endogenous production of the pro-inflammatory cytokine interleukin-6 (IL-6). Plasma lipid fractions, especially high density lipoproteins, bind and neutralize endotoxin and, therefore, inhibit endotoxin-induced macrophage cytokine production, including IL-6. Increased IL-6 plasma levels have been implicated in adverse consequences associated with CPB. Previous studies demonstrated large interpatient variability in IL-6 plasma levels after CPB. The purpose of this study was to evaluate the relationship between plasma lipid concentrations and the concentrations of IL-6 following CPB in humans.
Methods
In a prospective study, a group of 15 patients selected to exclude variables known to influence post-CPB plasma levels of IL-6 (preoperative left ventricular ejection fraction > 45%, similar durations of aortic cross clamping and total CPB time, similar temperature control during CPB, and avoidance of platelet transfusion and shed mediastinal blood re-infusion), IL-6 was measured at baseline, one and 24 hr post-CPB.
Results
Interleukin-6 plasma concentrations (mean ± SD) increased at one (142 ± 89 pg·ml−1,P < 0.05) and 24 (129 ± 82 pg·ml−1,P < 0.05) hr post-CPB compared with baseline (1,5 ± 1 pg·ml−1) concentrations. An inverse correlation was found between IL-6 plasma concentrations at one hour post-CPB and plasma cholesterol concentrations (r = -0.592,P = 0.02), high density lipoprotein (r = -0.595,P = 0.02), and low density lipoprotein (r = -0.656,P = 0.01).
Conclusions
These results suggest that plasma lipids attenuate the production of IL-6 during CPB and may partly explain the variability of interpatient levels of IL-6 reported post-CPB by others.
Résumé
Objectif
La circulation extracorporelle (CEC) est caractérisée par la translocation de l’endotoxine intestinale et la production endogène subséquente de la cytokine interleukine-6 (IL-6) pro-inflammatoire. Des fractions de lipides plasmatiques, surtout les lipoprotéines de haute densité, se fixent à l’endotoxine et la neutralisent et, par conséquent, inhibent la production de cytokine macrophage induite par l’endotoxine, incluant IL-6. Laccroissement des niveaux plasmatiques de IL-6 a été présumé comme responsable des conséquences défavorables associées à la CEC. Des études antérieures ont démontré une grande variabilité dans les niveaux plasmatiques de IL-6 à la suite d’une CEC. Le but de cette étude était d’évaluer la relation entre les concentrations de lipides plasmatiques et les concentrations de IL-6 après une CEC chez les humains.
Méthodes
Dans une étude prospective, un groupe de 15 patients a été sélectionné en excluant les variables connues pour influencer les niveaux plasmatiques de IL-6 post CEC (fraction d’éjection ventriculaire gauche préopératoire > 45%, durées similaires de clampage aortique et de temps total de CEC, contrôle similaire de la température pendant la CEC et suppression de la transfusion de plaquettes ainsi que de la reperfusion du sang médiastinal dérivé), IL-6 a été mesurée au début, puis une heure et 24 heures post CEC.
Résultats
Les concentrations plasmatiques d’inlerleukine-6 (moyenne ± écart type) s’accroissent à une heure (142 ± 89 pg·ml−1,P < 0,05) et à 24 heures (129 ± 82 pg·ml−1,P < 0,05) post CEC par rapport aux concentrations de base (1,5 ± 1 pg·ml−1). On a constaté une corrélation inverse entre les concentrations plasmatiques de IL-6 à une heure post CEC et les concentrations de cholestérol plasmatique (r = -0,592,P = 0,02), de lipoprotéines de haute densité (r = -0,595,P = 0,02) et de lipoprotéines de basse densité (r = -0,656,P = 0,01).
Conclusion
Ces résultats suggèrent que les lipides réduisent la production de IL-6 pendant la CEC et peuvent expliquer partiellement la variabilité interindividuelle des niveaux de IL-6 post CEC rapportés par d’autres chercheurs.
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Hill, G.E., Pohorecki, R. & Whitten, C.W. Plasma lipid concentrations correlate inversely with CPB-induced interleukin-6 release. Can J Anaesth 45, 509–514 (1998). https://doi.org/10.1007/BF03012699
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DOI: https://doi.org/10.1007/BF03012699