Tissue oxidative metabolism and microhemodynamics of the skin in rats exposed to stress factors of different duration and their combinations

Abstract

BACKGROUND: Changes in tissue oxidative metabolism (OM) under the action of stressors of different duration have not been studied. The question of the relationship of NADH and FAD coenzymes with the microcirculatory bed (MCB) remains open. AIM: The work is devoted to identifying the features of the reaction of skin microhemodynamics (MHS) and tissue OM in rats exposed to acute and chronic stress factors of different duration and their combinations. MATERIALS AND METHODS: The experiment was carried out on 100 male rats of the Wistar line weighing 200-220 g. The animals were divided into 5 groups of 20 rats. The 1st control group, the 2nd and 3rd groups were exposed to acute (AS) and chronic hypokinetic stress (HS), respectively; the 4th group (AS-HS) was previously exposed to AS (on the 1st day), and then to HS (1-10 days); 5-th group (for 10 days of the HS, then the impact of the AS on the 10th day). On the 10th day, the indicators of tissue OM and MHS were recorded. RESULTS: It was shown that AS and HS increase the requirement of cells for ATP and contribute to the predominance of oxidative phosphorylation (OPh) over other processes, as indicated by an increase in FAD. AS-HS significantly changes the OM, separating the OPh and activating glycolysis. HS-AS does not cause such changes. AS increases the microcirculation index (MI) and reduces the coefficient of variation (Cv), HS reduces the MI and increases the mean square deviation (MSD). AS-HS significantly increases MI, and HS-AS MSD and Cv, but reduces MI. CONCLUSIONS: AS and HS increase the requirement of cells for ATP and contribute to the predominance of OPh over other processes. AS-HS modifies OM, disconnecting OPh and activating glycolysis. HS-AS depletes the metabolic reserves of the body. AS-HS rearranges metabolism along the path of glycolysis, protecting against stress factors and preventing the development of oxidative stress. AS leads to hyperemia and stasis of blood circulation in the microarray, reducing vasomotor activity of vessels. HS inhibits the level of tissue perfusion, reduces the inflow of arterial blood into the MCB and the outflow of venous blood, leading to spastic, stagnant phenomena and stasis. AS-HS reduces vasoconstriction, preparing the MCB for prolonged hypokinesia. HS-AS levels vasodilation, improves the parameters of MHS (MSD and Cv).