The Nature of Destructive and Compensator-Restorative Processes in the Rat Heart Myocardium after a Traumatic Brain Injury Performing Various Physical Exercises
Traumatic Brain Injury (TBI) is one of the most common causes of disability and is an economic burden for society. The pathophysiological mechanisms of brain damage in TBI are based on the action of primary and secondary damaging factors. Secondary injuries are cascading biochemical, inflammatory, stress reactions, one of which is nonspecific systemic activation of hemostasis caused by hypoxia, an increase in free reactive oxygen species, a slowdown in blood flow, an increase in blood viscosity. The primary aim of this article is to examine the nature of destructive and compensatorrestorative processes in the rat heart myocardium after a traumatic brain injury performing various physical exercises. To meet the aim of the study, some experiments have been carried out on outbred laboratory albino rats aged from 21 to 210 days. Meanwhile, the basis for the age periodization of rats is the anatomical and physiological characteristics of animals. The results of the experiments demonstrate that the group of animals with Unlimited Motor Activity (UMA) after 30 days have no recovery of the parameters of cellular structures to the values of the control group. Furthermore, over the first day after modeling the traumatic brain injury, all age groups of experimental animals manifest a decrease in the number of intact neurons and an increase in the number of degenerative changed neurons. Consequently, it can be concluded most desirable mode of physical activity for rats of all age groups is the performance of dynamic exercises in the form of systematic swimming.