TITLE

Endotoxin in pooled pericardial blood contributes to the systemic inflammatory response during cardiac surgery

AUTHOR(S)
Spanier, T.; Tector, K.; Schwartz, G.; Chen, J.; Oz, M.; Beck, J.; Mongero, L.
PUB. DATE
September 2000
SOURCE
Perfusion;Sep2000, Vol. 15 Issue 5, p427
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Although endotoxin has been implicated as an important contributor to the systemic inflammatory response (SIR) during cardiopulmonary bypass (CPB), its source remains unclear. While gut translocation has traditionally been perceived as the primary source of endotoxemia, accumulation of endotoxin in pooled pericardial blood may represent an additional source of endotoxin that is continually reinfused into the CPB circuit. Eighteen patients undergoing primary coronary revascularization procedures were prospectively evaluated. Shed blood pooled in the pericardial space was returned to the CPB circuit through cardiotomy suction catheters at 45 min after placement of the aortic crossclamp. Simultaneous samples of pooled pericardial and peripheral arterial blood were obtained and analyzed by a limulus amebocyte lysate assay for the determination of endotoxin concentration, and an enzyme-linked immonosorbert assay for tumor necrosis factor (TNF-a) levels. Significant elevations in endotoxin were demonstrated in pooled pericardial blood samples compared with arterial blood (3.5 ± 0.5 vs 0.8 ± 0.2 pg/ml; p < 0.05). TNF-a levels were below the limits of detection in both samples. These data implicate pooled pericardial blood as an important primary source of endotoxin that, when continually reinfused throughout CPB, may contribute to the overall SIR. Because endotoxemia has been identified as an important predictor of adverse outcomes following cardiac surgery, removal of endotoxin antigen in shed pericardial blood, prior to its reinfusion into the CPB circuit, may provide a directed means to improve perioperative outcome without compromising established blood conservation techniques.
ACCESSION #
3591943

 

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