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Early changes in plasma antioxidant and lipid peroxidation levels following coronary artery bypass surgery: a complex
Leon Hadjinikolaou1, Christos Alexiou, Andrew S Cohen
1Academic Department of Cardiac Surgery, Glenfield General Hospital, University of Leicester, Groby Road, LE3 9QP, Leicester, UK.
Objective:
Total plasma antioxidant capacity (TPAC) quantitatively defines extracellular fluid antioxidant capacity, the mechanism of which is different from the intracellular mechanism. Patients undergoing surgery for congenital heart defects have suppressed TPAC in the early postoperative periods. Our aim was to study the early changes of TPAC following coronary artery bypass grafting (CABG), in relation to lipid peroxidation, and to identify clinical factors affecting these changes.
Methods:
We studied 28 consecutive patients undergoing routine uncomplicated CABG with cardiopulmonary bypass (CPB). Patients taking known antioxidants, such as captopril and allopurinol, and those receiving transfusion of blood or blood products at operation or during the first 72 postoperative hours were excluded. Serial blood samples were obtained for TPAC and lipid hydroperoxide concentration (LPX).
Results:
TPAC was suppressed for 72 h after the operation, while LPX exhibited a significant increase only 1 h post-operatively. TPAC time changes resulted from a simultaneous depression (50% of the baseline occurring approximately 6 h after the operation) and production (18% of the baseline occurring approximately 6 h after the operation) of plasma antioxidants. The earlier the peak of plasma antioxidant production the later and the less the plasma antioxidant depression. Plasma antioxidant depression was inversely related to LPX (r=-0.37, P=0.05 and r=-0.40, P=0.04 at 1 and 6 h respectively). Ejection fraction and operative myocardial ischaemic times significantly influenced plasma antioxidant depression.
Conclusions:
TPAC is suppressed for 72 h following CABG. TPAC depression may be involved in the mechanism of lipid peroxidation and is influenced by clinical factors known to be related to post CABG morbidity and mortality, like low ejection fraction and long ischaemic times.