Abstract
BackgroundHeatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Previously proposed animal models of heatstroke disregard the impact of RH. Therefore, we aimed to establish and validate an animal model of heatstroke considering RH. To validate our model, we also examined the effect of hydration and investigated gene expression of cotransporter proteins in the intestinal membranes after heat exposure.MethodsMildly dehydrated adult male C57/BL6J mice were subjected to three AT conditions (37 °C, 41 °C, or 43 °C) at RH > 99% and monitored with WetBulb globe temperature (WBGT) for 1 h. The survival rate, body weight, core body temperature, blood parameters, and histologically confirmed tissue damage were evaluated to establish a mouse heatstroke model. Then, the mice received no treatment, water, or oral rehydration solution (ORS) before and after heat exposure; subsequent organ damage was compared using our model. Thereafter, we investigated cotransporter protein gene expressions in the intestinal membranes of mice that received no treatment, water, or ORS.ResultsThe survival rates of mice exposed to ATs of 37 °C, 41 °C, and 43 °C were 100%, 83.3%, and 0%, respectively. From this result, we excluded AT43. Mice in the AT 41 °C group appeared to be more dehydrated than those in the AT 37 °C group. WBGT in the AT 41 °C group was > 44 °C; core body temperature in this group reached 41.3 ± 0.08 °C during heat exposure and decreased to 34.0 ± 0.18 °C, returning to baseline after 8 h which showed a biphasic thermal dysregulation response. The AT 41 °C group presented with greater hepatic, renal, and musculoskeletal damage than did the other groups. The impact of ORS on recovery was greater than that of water or no treatment. The administration of ORS with heat exposure increased cotransporter gene expression in the intestines and reduced heatstroke-related damage.ConclusionsWe developed a novel mouse heatstroke model that considered AT and RH. We found that ORS administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines.
Highlights
Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death
We found that oral rehydration solution (ORS) administration improved inadequate circulation and reduced tissue injury by increasing cotransporter gene expression in the intestines
The International Labour Organization has reported that AT is estimated to increase by 1.5–3.0 °C by 2100, which would result in increased frequency and severity of heatstroke worldwide; heatstroke-associated economic losses are expected to exceed 2.4 billion USD by 2030 [3, 4]
Summary
Heatstroke is associated with exposure to high ambient temperature (AT) and relative humidity (RH), and an increased risk of organ damage or death. Heatstroke is caused by exposure to high ambient temperature (AT) and can cause organ damage or death [1, 2]. Heat exposure is associated with damage to organs including the heart, lung, liver, kidney, gastrointestinal tract, muscle, and central nervous system. It can induce systemic inflammatory response syndrome, which may lead to multiple organ dysfunction or death [1, 2, 5]. During exposure to high AT, the human body triggers heat divergence processes, including diaphoresis, increased respiratoryrate, and vasodilation, aiming to maintain the baseline cT. People feel hotter in high ATs and RH than they would in dry conditions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
