Abstract
White male Wistar rats were cooled in water (9–10°C) to respiratory arrest (rectal temperature 14.7 ± 0.5°C, brain temperature 16.0 ± 0.3°C). After removal from water, animals received intravenous 0.5% ethylenediaminetetraacetic acid disodium salt (Na2EDTA) to decrease the blood Ca2+ concentration. Respiration was reinitiated 4–8 min after administration of Na2EDTA. One group of rats was then further cooled to a body temperature of 12.2 ± 0.7°C (brain temperature 14.9 ± 0.3°C); at these low temperatures, rats maintained respiration at a level of 12 ± 3 cycles/min for 2–3 h. After restarting respiration, rats of group 2 were not subjected to further cooling, and the same dose of Na2EDTA, at rectal and brain temperatures of 15–16°C, increased respiratory rate to the higher level of 29 ± 4 cycles/min. Administration of Na2EDTA into the circulatory system of hypothermic rats evidently slowed the process of accumulation of Ca2+ in the cytoplasm of respiratory center cells, impairing their functioning. These results suggest that in hypothermia, injection of Na2EDTA activates the mechanisms protecting cells from cold injury. These results, along with published data, lead to the conclusion that non-hibernating homeothermic organisms are able to maintain the main vital functions at signifi cantly reduced body temperatures.
Published Version
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