Antioxidant-Prooxidant Alterations of Propofol in New Zealand White Rabbits

Long-term administration of anaesthetic drugs can cause the accumulation of free radicals in the blood and vital organs. This study investigated the anaesthetic effects of long-term administration of propofol (2-6-diisopropylphenol) for deep sedation, on oxidative biomarkers in New Zealand white rabbits. Animals were randomly divided into four groups: control group and three experimental groups (n=6). All experimental groups were anesthetized intramuscularly with 5 mg/kg b.wt. xylazine and 40mg/kg b.wt. ketamine HCl. After sedation with xylazine, an intravenous catheter was inserted and then propofol infusion (for an hr; 40-50mg/kg/hr b.wt., following doses as 30,25 and 20mg/kg/h b.wt) was started via a perfusion pump. In the control group, no propofol infusion was administered, and blood samples were taken after ketamine-induction. The experimental groups received propofol infusion through the ear vein for 6,12, and 24-hrs. Blood samples were collected after anaesthesia period in each group just before euthanasia. Following euthanasia, tissue samples were collected. Alterations in lipid and protein oxidation, antioxidant capacity, glutathione levels, and catalase activity were evaluated in the blood and tissue samples. Additionally, principal component analysis and multivariate correlation analysis were applied to interpret the results. The results demonstrated that serum protein oxidation increased by 135.9% with prolonged propofol exposure indicating free radical formation (p<0.05). Notably, oxidative stress was most pronounced in brain tissue during prolonged deep sedation induced by propofol. These finding suggest that monitoring of oxidative stress markers enables the detection of metabolic disturbance that may occur in patients, facilitating early intervention, and potentially reducing mortality.