Large temperature fluctuations and climate changes affect the global temperature, with the period between 2011 and 2020 being the warmest in the last 140 years (14–17). Since 2015, the warmest years are 2016, ,2019, and 2020. The mean global temperature was 1.2°C above the level in 2020, (17) and between 2030 and 2052, it is predicted to rise by another 1.5°C (18). These temperature changes in the environment directly affect the internal temperature of the organism because the basic temperatures increase and the loss of water in the body also increases the reserve consumption of the compensatory mechanisms of the organism (18).
Heatstroke leads to oxidative cellular stress and impaired thermocompensatory mechanisms, and can range from subtle heat exhaustion to death. The organism includes compensatory mechanisms of heat release through sweating, tachycardia, and ultimately the activation of pro-inflammatory and inflammatory cytokines. Heatstroke is defined as a state of elevated body temperature of 40.05°C and above this value, which is a consequence of overemphasized compensatory mechanisms and exhausted body reserves with interindividual variations (19,2Heatheat stroke, a condition occurs in the range of 10 to 50% leads to death through cardiac dysfunction with global hypokinesia (21). Given that the number of deaths caused by heatstroke is increasing, it is necessary to understand the behavioral response of the organism to increased environmental temperature, which is directly related to global warming (22). In the world, the number of deaths that occur in closed spaces with an increase in air temperature inside the room, for example during bathing, in saunas, Turkish baths, and among athletes due to strenuous training, especially in the summer months, is increasing. Two significant causes of sudden death in athletes are death due to arrhythmia and heat stroke. Death caused by arrhythmia is mate in the center of medical attention while heatstroke is less considered (23). Autopsy rates remain low and vary between countries, and protocols for performing autopsies in cases of suspected sudden death also differ (24).
Determining heat stroke as the cause of death is very difficult in forensic medicine due to the non-specificity of biochemical analyses. In our rat model of thermal climate, a thermoregulatory response was included by exposing rats to different water temperatures (37, 41, and 44°C). An esophageal probe was used to measure core temperature. The proven physiological body temperature of rats is 37.5–37.7°C (25), the research aim was to determine the core values of rats exposed to different water temperatures (37, 41, and 44°C), before the start of the experiment (Tb), after immersion after (Tu), after 20 minutes of exposure (Tu) and at the moment of death. (Ts) rats of hyperthermia and heat stroke basalasal temperature was the lowest in group G44 and the highest in the control group, which is in correlation with interindividual variations. The death temperature was lower in G41 compared to G44, which prese of the physiological state and the absence of pathological processes in the rats before the experiment started. Given that the analysis of basal temperatures in the grower was not significant, this points to the conclusion about the organism's physiological state and normothermia in rats before the start of the experiment. A significant difference appears during water immersion, after 20 minutes, and at the moment of death, which points to the control mechanisms of the thermoregulation center. Heat stroke was detected in rats exposedtheto the highest temperature of 44 degrees.
Our results with the literature data that indicate that the minimum time required for the onset of heatstroke, with the compensatory mechanisms of the organism involved, is 20 minutes from the moment of the target temperature (19). Basal temperature is the result of the organism's physiological thermoregulation itself, while increased ambient temperature and the length of exposure of the body affect the increase in internal temperature and the inclusion of the compensatory mechanisms of the organism with the exchange of heat between the body and the environment. The temperature of rats at the time of death was 44.02 ± 0.38°C in group G44-heat stroke, and 41.20 ± 0.76°C in G41. The rats exposed to water temperatures of 41°C and 44°C had longer survival in group G41 175.50 minutes, compared to rats in group G44 4.14 minutes (p = 0.001), therefore, the shperiodriod of exposure to high temperature caused that there were more rats of group 44 that did not reach the temperature threshold for heat stroke. In a study by Quinn et al. (26), a predetermined temperature is used as the temperature standard of heatstroke, which was also done in our research, and is considered an interindividual variation (27–30). In a study of healthy individuals, the internal temperature reached values of 40°C after 10 minutes of exposure. In addition, deterioration of brain and heart function was observed after immersion in water at a temperature of 44°C, but no brain and heart damage was observed after immersion in water heated to 40°C. The degree of damage depends on the temperature of the environment and the length of exposure of the body to that environment (30). Heat stress induces systemic inflammation through increased cytokine and white blood cell concentrations, which contributes to hyperthermia and reduced metabolic activities, as metabolic reservoirs are depleted to deploy homeostatic mechanisms. Excessive inflammation in heat stress induces the release of damage-associated molecular ligands from apoptotic cells in the final stage of pyroptosis (31).
The modern epoch of climate change also caused research on the topic of thermoregulation of the organbywith adaptation to high temperatures. Thermoregulation of heat is described by the central integrator model of peripheral and central heat inputs that activate thermoeffector reactions when the core temperature moves above physiological. However, further research should consider more complex models that include several integrators and other afferent signals taking into account the stages of the heat flow mechanism and the interindividual variations of the response that cannot be excluded.