The aim of this study was revealing the temperature changes in rats' brain tissue caused by whole body hyperthermia. The analysis of received results allows to conclude that the brain has a highly secured system of temperature autoregulation against the exogenous temperature changes. The upper limit of this autoregulation (for rats, at least) is in the range of 45°C of environment. An important role in the normal functioning of the brain temperature autoregulation system belongs to Nitric Oxide. The behavioral disorders, observed in animals after whole body hyperthermia (sure within the range of brain temperature autoregulation) are hardly associated with the changes in temperature of the Central Nervous System, but rather have to be mediated by impaired blood circulation and oxygen supply to the brain tissues, caused by the rapid deterioration of the blood rheological properties. 1. Introduction In our previous experimental studies significant morphophysiological changes in the rats’ brains tissue caused by local hyperthermia (43°C, 60？min. exposure) have been revealed [1, 2]. On Figure 1 we can see the clear-cut edge of damaged tissue in the rat’s cerebral cortex. Analysis of the results allowed us to conclude that in the development of these changes essential role belongs to the mechanism associated with intense activation of Nitric Oxide Synthases (NOS), resulting (in the initial phase of hyperthermic exposure) in increased oxygenation of exposed brain tissue, and then (in the second phase of exposure), to changes in blood rheological properties resulting in thrombosis of cerebral vessels [3]. Figure 1: Sensory-motor cortex of rats’ brain; 60 minutes hyperthermia (43°C); arrows show the clear-cut edge of damaged tissue. Confirmation of this conclusion is presented in Figures 2(a) and 2(b). In Figure 2(a) we can see a sensory-motor cortex of rats’ brains with a lot of thrombosed cerebral vessels after 60 minutes of hyperthermic exposure in control rats brains, and in Figure 2(b), the similar picture in experimental rats’ brains with inhibited production of Nitric Oxide, we can see just a single thrombosed cerebral vessels. Figure 2: Sensory-motor cortex of normal (a) and L-NAME injected (b) rats’ brain; 60-minute hyperthermia (43°C). In the case of tumor tissue, we believe that the initial thermal hyperemia leads to a deterioration in the process of glycolysis due to increased oxygenation of tissues (Pasteur effect), and subsequent thrombosis leads to the sharp decrease in glucose delivery to tumor cells and to their unconditional death. Based on the
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