OBJECTIVE AND DESIGN: The beneficial effects of leukocyte filtration on the outcome of cardiac surgery with cardiopulmonary bypass (CPB) is probably due to the limitation of pathogenesis mediated by over-stimulated neutrophils. However, the influence of leukocyte filtration on the functional neutrophil activity has not been studied in detail. Therefore, by using different filtration timing strategies we determined neutrophil effector functions before and after the filter passage as well as blood surrogate markers for neutrophil activation. METHODS: We randomly assigned 80 cardiac surgery patients to four groups (n = 20 each) without (1) and with three different filtration timing strategies (II-IV). As functional end points neutrophil phagocytic activity and oxidative burst upon ex vivo stimulation with E.coli were analyzed from blood of 31 patients whereas polymorphonuclear elastase (PMNE), myeloperoxidase, and malondialdehyde (MDA), a marker for lipid peroxidation was determined in plasma samples from 80 patients. Blood was harvested immediately before and behind the filter (Pall LG6) at different times during CPB. RESULTS: We found that none of the filtration strategies either reduced the number of neutrophils capable of eliciting phagocytic activity and oxidative burst or the activity per cell. In contrast, PMNE and MPO levels in peripheral venous blood were found to be significantly increased in groups II-IV compared with group I throughout the entire filtration period in all patients. MDA was not enhanced in the filter groups. CONCLUSIONS: Our results show that the leukocyte depletion filter in the arterial line of the heart-lung machine failed to limit neutrophil stimulation but rather augmented PMNE plasma levels. We speculate that augmented PMNE and MPO levels mainly stem from neutrophils that are captured within the mesh of the leukocyte filter.
RCT Entities:
OBJECTIVE AND DESIGN: The beneficial effects of leukocyte filtration on the outcome of cardiac surgery with cardiopulmonary bypass (CPB) is probably due to the limitation of pathogenesis mediated by over-stimulated neutrophils. However, the influence of leukocyte filtration on the functional neutrophil activity has not been studied in detail. Therefore, by using different filtration timing strategies we determined neutrophil effector functions before and after the filter passage as well as blood surrogate markers for neutrophil activation. METHODS: We randomly assigned 80 cardiac surgery patients to four groups (n = 20 each) without (1) and with three different filtration timing strategies (II-IV). As functional end points neutrophil phagocytic activity and oxidative burst upon ex vivo stimulation with E.coli were analyzed from blood of 31 patients whereas polymorphonuclear elastase (PMNE), myeloperoxidase, and malondialdehyde (MDA), a marker for lipid peroxidation was determined in plasma samples from 80 patients. Blood was harvested immediately before and behind the filter (Pall LG6) at different times during CPB. RESULTS: We found that none of the filtration strategies either reduced the number of neutrophils capable of eliciting phagocytic activity and oxidative burst or the activity per cell. In contrast, PMNE and MPO levels in peripheral venous blood were found to be significantly increased in groups II-IV compared with group I throughout the entire filtration period in all patients. MDA was not enhanced in the filter groups. CONCLUSIONS: Our results show that the leukocyte depletion filter in the arterial line of the heart-lung machine failed to limit neutrophil stimulation but rather augmented PMNE plasma levels. We speculate that augmented PMNE and MPO levels mainly stem from neutrophils that are captured within the mesh of the leukocyte filter.
Authors: S M Muro; J H Lee; J V Stokes; M K Ross; T M Archer; R W Wills; A J Mackin; J M Thomason Journal: J Vet Intern Med Date: 2017-01-31 Impact factor: 3.333
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Authors: Ulf Abdel-Rahman; Stefan Margraf; Tayfun Aybek; Tim Lögters; José Bitu-Moreno; Ieda Francischetti; Tilmann Kranert; Frank Grünwald; Joachim Windolf; Anton Moritz; Martin Scholz Journal: J Inflamm (Lond) Date: 2007-10-10 Impact factor: 4.981