Association of Hyperlactatemia and IL-6 Hypercytokinemia after Cardiopulmonary Bypass -A Preliminary Report-
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Background: In cardiac surgery with cardiopulmonary bypass (CPB), hyperlactatemia (HL) is common and is associated with postoperative morbidity and mortality. At present, the cause of HL during CPB is proposed to be tissue hypoxia. Tissue perfusion and oxygen delivery can be impaired to varying degrees during CPB. Although surgery involving CPB apparatus is associated with increased pro-inflammatory mediators, such as TNF-α and IL-6, tissue hypoxia that occurs during CPB may be an additionally potent stimulus to inflammation. We hypothesized that hypoxic patients during CPB that experience elevated serum lactate levels, may be related to higher serum cytokine level after CPB than normoxic patients during CPB with normal serum lactate levels. Methods: Levels of TNF-α and IL-6 were measured by ELISA in a) Time 1; before initiation of CPB, b) Time 2; 30 min after aortic de-clamping, c) Time 3; 24 hrs after aortic de-clamping. Levels of lactate was measured at a) Time A; before initiation of CPB, b) Time B; 30 min after aortic de-clamping. Postoperative ICU stay, intubation time and oxygen index were evaluated as postoperative morbidity scale. Results: There were no statistical differences between HL (n = 43, lactate ≥3 mMol/L at time B) and normal lactate group (NL) (n = 63, lactate ＜3 mMol/L at time B) in demographic data, preoperative left ventricular ejection fraction, CPB time, and aortic cross-clamp time. Level of IL-6 in HL at time 3 was higher than that of NL. The ICU stay and intubation time were longer in HL. The oxygen index on 1st postoperative day was lower in HL. Conclusions: Our results suggest that hyperlactatemia after weaning from CPB may be related to IL-6 hypercytokinemia, and therefore related to postoperative morbidity.
Abstract
Background: In cardiac surgery with cardiopulmonary bypass (CPB), hyperlactatemia (HL) is common and is associated with postoperative morbidity and mortality. At present, the cause of HL during CPB is proposed to be tissue hypoxia. Tissue perfusion and oxygen delivery can be impaired to varying degrees during CPB. Although surgery involving CPB apparatus is associated with increased pro-inflammatory mediators, such as TNF-α and IL-6, tissue hypoxia that occurs during CPB may be an additionally potent stimulus to inflammation. We hypothesized that hypoxic patients during CPB that experience elevated serum lactate levels, may be related to higher serum cytokine level after CPB than normoxic patients during CPB with normal serum lactate levels. Methods: Levels of TNF-α and IL-6 were measured by ELISA in a) Time 1; before initiation of CPB, b) Time 2; 30 min after aortic de-clamping, c) Time 3; 24 hrs after aortic de-clamping. Levels of lactate was measured at a) Time A; before initiation of CPB, b) Time B; 30 min after aortic de-clamping. Postoperative ICU stay, intubation time and oxygen index were evaluated as postoperative morbidity scale. Results: There were no statistical differences between HL (n = 43, lactate ≥3 mMol/L at time B) and normal lactate group (NL) (n = 63, lactate ＜3 mMol/L at time B) in demographic data, preoperative left ventricular ejection fraction, CPB time, and aortic cross-clamp time. Level of IL-6 in HL at time 3 was higher than that of NL. The ICU stay and intubation time were longer in HL. The oxygen index on 1st postoperative day was lower in HL. Conclusions: Our results suggest that hyperlactatemia after weaning from CPB may be related to IL-6 hypercytokinemia, and therefore related to postoperative morbidity.
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