Abstract
METHODS: To investigate how the timing of cooling therapy affects organ injuries in rats with exertional heat stroke (EHS) and explore the possible mechanisms. METHODS: A total of 60 adult male Wistar rat models of EHS were randomized into model group without active cooling after modeling, immediate cooling group with cold water bath immediately after modeling, delayed cooling groups with cold water bath at 5, 15 and 30 min after modeling, with another 12 mice without EHS as the normal control group. The changes in core body temperature of the mice were recorded and the cooling rate was calculated. After observation for 24 h, the mice were euthanized and blood samples were collected for detection of interleukin-1β (IL-1β), IL-2, IL-4, IL-6, IL-10, and interferon-γ, followed by pathological examination of the vital organs. The rats that died within 24 h were immediately dissected for examination. RESULTS: The number of deaths of the model rats within 24 h increased significantly with the time of delay of cooling treatment. The delay of cooling was positively correlated (r=0.996, P=0.004) while the cooling rate negatively correlated with the mortality rate (r=-0.961, P=0.009). The inflammatory cytokine levels presented with different patterns of variations among the cooling intervention groups. All the rat models of EHS had significant organ damages characterized mainly by epithelial shedding, edema, effusion, and inflammatory cell infiltration, and brain and renal injuries reached the peak level at 24 h after EHS. CONCLUSION: EHS causes significant nonspecific pathologies of varying severities in the vital organs of rats, and the injuries worsen progressively with the delay of cooling. There is a significant heterogeneity in changes of serum inflammatory cytokines in rats with different timing of cooling intervention following EHS.