Вплив лапаратомії та ліпополісахаридіндукованої системної запальної відповіді на метаболічні розлади в організмі щурів

Abstract

This investigation is aimed at studying the effect of abdominal surgical trauma (laparotomy) on markers of surgical stress and acute phase response as well as markers of carbohydrate and lipid metabolism under lipopolysaccharide (LPS) -induced systemic inflammatory response (SIR). Male Wistar rats were divided into 4 groups: 1st (control) group included “pseudooperated” animals (the procedure included the administration of anesthesia, epilation, fixation of animals, compression of the skin of the abdomen with Mikulicz’s clamp by one click); the 2nd group included the rats, which were injected Salmonella typhi (in a dose of 0.4 μg/kg body weight 3 times during the 1st week and once a week for the next 7 weeks) before performing the “false operation”; the 3rd group was made up of the rats after laparotomy; and the 4th group involved the rats after laparotomy performed under LPSinduced SIR. The markers were assessed in 7 days following the “pseudo-operation” or laparotomy. The results obtained have demonstrated the combined effect of laparotomy and LPS-induced SIR was accompanied by a significant increase in the marker of surgical stress, the concentration of cortisol in blood plasma, which significantly exceeded the values of the groups 2 and 3 – by 61.8 and 25.1%, respectively. However, the content of acute-phase protein ceruloplasmin, an acute phase reactant, in the serum remained at the level of the 2nd group. Under these conditions, the concentration of very low-density lipoprotein cholesterol and triglycerides significantly exceeded the relevant values in the 2nd and 3rd groups. The combined effect of surgical trauma and LPS-induced SIR considerably reduced the activity of constitutive isoforms of NO-synthase, which was significantly lower, by 41.7%, than the value in the group 2, and by 41.7% lower than in the group 3. At the same time, the total activity of this enzyme and the activity of its inducible isoform were consistent with the values of the 2nd group. This was accompanied by the development of decompensated lipid peroxidation (with a considerable decrease in the blood antioxidant potential).