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CLINICAL TRIAL
COMPARATIVE STUDY
JOURNAL ARTICLE
RANDOMIZED CONTROLLED TRIAL
IL-6 and IL-8 levels after cardiopulmonary bypass are not affected by surface coating.
Annals of Thoracic Surgery 1999 November
UNLABELLED: BACKGROUND.:Contact of blood with the surfaces of the cardiopulmonary bypass (CPB) circuit has been implicated as a cause of the inflammatory response. We undertook a prospective randomized trial of 200 pediatric patients, all with a calculated total bypass flow of less than 2.3 L/min (< 0.96 L/m2/min).
METHODS: Patients were randomly assigned to 1 of 4 CPB groups: (1) Nonheparin-bonded circuit with no albumin preprime; (2) Nonheparin-bonded circuit with albumin preprime; (3) Heparin-bonded circuit with no albumin preprime; (4) Heparin-bonded circuit with albumin preprime. Measurements of cytokines, (interleukin [IL]-6, IL-8) and blood cell counts were made prebypass and 6 and 24 hours after institution of cardiopulmonary bypass.
RESULTS: Analysis of variance showed no significant difference in any of the clinical or biochemical characteristics of the 4 groups. The interaction between heparin-bonded oxygenators and albumin preprime was not significant. No important differences in IL-6 or IL-8 concentrations were noted after CPB using either heparin or nonheparin-bonded oxygenators with albumin or albumin free preprime using two-way analysis of variance.
CONCLUSIONS: Albumin preprime and heparin-bonding do not attenuate the inflammatory response component attributable to the concentration of these markers.
METHODS: Patients were randomly assigned to 1 of 4 CPB groups: (1) Nonheparin-bonded circuit with no albumin preprime; (2) Nonheparin-bonded circuit with albumin preprime; (3) Heparin-bonded circuit with no albumin preprime; (4) Heparin-bonded circuit with albumin preprime. Measurements of cytokines, (interleukin [IL]-6, IL-8) and blood cell counts were made prebypass and 6 and 24 hours after institution of cardiopulmonary bypass.
RESULTS: Analysis of variance showed no significant difference in any of the clinical or biochemical characteristics of the 4 groups. The interaction between heparin-bonded oxygenators and albumin preprime was not significant. No important differences in IL-6 or IL-8 concentrations were noted after CPB using either heparin or nonheparin-bonded oxygenators with albumin or albumin free preprime using two-way analysis of variance.
CONCLUSIONS: Albumin preprime and heparin-bonding do not attenuate the inflammatory response component attributable to the concentration of these markers.
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