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

BACKGROUND: Changes in tissue oxidative metabolism under the action of stressors of different durations have not been studied. The relationship between NADH and FAD coenzymes and the microcirculatory bed remains unclear.

AIM: This study aimed to identify the features of the reaction of skin microhemodynamics and tissue oxidative metabolism in rats exposed to acute and chronic stress factors of different durations and their combinations.

MATERIALS AND METHODS: The experiment was performed on 100 male Wistar rats weighing 200–220 g. The animals were divided into five groups of 20 rats. The first control group and the second and third groups were exposed to acute stress (AS) and chronic hypokinetic stress (HS), respectively; the fourth group (AS-HS) was previously exposed to AS (on the first day) and then to HS (1–10 days); and the fifth group (for 10 days of the HS, then the effect of the AS on day 10). On day 10, the indicators of tissue oxidative metabolism and skin microhemodynamics were recorded.

RESULTS: AS and HS increased the requirement of cells for ATP and contributed to the predominance of oxidative phosphorylation over other processes, as indicated by an increase in FAD. AS-HS significantly changed oxidative metabolism, separating oxidative phosphorylation and activating glycolysis. HS-AS did not cause such changes. AS increased the microcirculation index and reduced the coefficient of variation, and HS reduced the microcirculation index and increased the mean square deviation. AS–HS significantly increased the microcirculation index, and HS-AS increased the mean square deviation and coefficient of variation but reduced the microcirculation index.

CONCLUSIONS: AS and HS increase the requirement of cells for ATP and contribute to the predominance of oxidative phosphorylation over other processes. AS-HS modifies oxidative metabolism by disconnecting oxidative phosphorylation 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 the vasomotor activity of the vessels. HS inhibits the level of tissue perfusion and reduces the inflow of arterial blood into the microcirculatory bed and the outflow of venous blood, leading to spastic, stagnant phenomena and stasis. AS-HS reduces vasoconstriction, preparing a microcirculatory bed for prolonged hypokinesia. HS-AS levels vasodilation and improves the parameters of skin microhemodynamics (mean square deviation and coefficient of variation).