Oxidative stress and hepatic monooxygenase function in patients with coronary heart disease before and after cardiac surgery

The parameters of lipid peroxidation (LPO) and hepatic monooxygenase function (HMF) were studied in 92 patients with coronary heart disease (CHD). After termination of and within the first 24 hours after myocardial revascularization, the levels of malonic dialdehyde and conjugate trienes were found to show 45.6 and 62.1% increases, respectively. The half-life of antipyrine (AP T(1/2)) increased by 23.5%. Studies on postoperative days 3-4 and 10-12 revealed a reduction in LPO rates and normalized HMF. After off-pump surgery, LPO and HMF significantly unchanged. On the contrary, open heart surgery resulted in a noticeable activation of LPO and an almost 1.5-fold decrease in HMF. The increase in oxidative stress and the deceleration of hepatic microsomal oxidation were ascertained to be directly related to the duration of extracorporeal circulation and the time of myocardial ischemia. After surgery, the rate of LPO and the reduction of HMF were more considerable in patients with multiple organ dysfunctions, as compared with the uncomplicated postoperative period. Within the first 24 hours following surgery, AP T(1/2) increased by 83.4%, but on postoperative days 10 to 14, it remained to be decreased by almost 1.5 times as compared with the baseline. Thus, LPO activation is one of the leading mechanisms of decelerated hepatic xenobiotic biotransformation after myocardial revascularization. Diminished lower HMF enhances the sensitivity of CHD patients to drug therapy and requires a differential approach to its use.