Oxidative stress and liver monooxygenase function after heart valve surgery

Abstract

Background and objectives: this prospective study was carried out to evaluate oxidative stress and liver monooxygenase function after cardiac surgery in patients with acquired valvular heart disease. Methods: 97 patients were studied. Oxidative stress was quantified with malondialdehyde, coupled trienes, hepatocuprein, and catalase activity. Liver monooxygenase function was evaluated with antipyrine pharmacokinetics. For statistical analyses, the Dunnett test and Pearson’s correlation coefficient were used. Results: on the 1st–2nd postoperative days, high lipid peroxidation activation (malondialdehyde: 9.6 ± 2.7 vs. 6.9 ± 2.0 nmol·mL−1, p < 0.05) and a significant decrease in liver monooxygenase function (antipyrine clearance: 18.3 ± 11.1 vs. 39.0 ± 18.9 mL·kg−1·h−1, p < 0.05) were revealed. On the 3rd–4th and 11th–12th postoperative days, the intensity of oxidative stress decreased and monooxygenase function returned to baseline (antipyrine clearance: 45.6 ± 17.9 vs. 39.0 ± 18.9 mL·kg−1·h−1). The analysis showed a negative relationship between oxidative stress and liver monooxygenase function. Conclusion: patients undergoing surgery for acquired valvular heart disease have considerable oxidative stress and a decrease in liver monooxygenase function on the 1st–2nd postoperative days. Activation of lipid peroxidation is one of the main reasons for suppression of microsomal monooxygenases activity. A slowdown of liver microsomal oxidation might change the pharmacokinetic response of patients under drug therapy.