Abstract

Purpose: to study ischemic depolarization in focal cerebral ischemia in rats.Materials and methods. We conducted simulations of focal cerebral ischemia in 30 rats. The animals were divided into three groups: 1) normothermia (n = 10), 2) hypothermia (n = 10), 3) hyperthermia (n = 10). We identified a statistically significant correlation between the animal's body temperature and the number of episodes of depolarization. (r = 0,87, p<0,001). The average number of DC potential deviations in animals with hyperthermia was statistically significantly higher than in animals with normothermia. (p<0,05).Results. Tissue damage as a result of focal cerebral ischemia correlates with body temperature fluctuations. A decrease in body temperature in focal cerebral ischemia leads to a decrease in the size of the ischemia zone, and as a result of a cerebral infarction, and vice versa, a slight increase in body temperature leads to an increase in the area of cerebral infarction.Conclusion. On tissue, temperature fluctuations have physiological and biochemical effects, a statistically significant correlation between episodes of depolarization in cerebral ischemia and the percentage of brain damage after ischemia are not always in a cause-and-effect relationship.

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