Miyamoto Kazuyuki, Suzuki Keisuke, Ohtaki Hirokazu, Nakamura Motoyasu, Yamaga Hiroki, Yagi Masaharu, Honda Kazuho, Hayashi Munetaka, Dohi Kenji
Department of Emergency, Critical Care and Disaster Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan.
Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-Ku, Tokyo, 142-8555, Japan.
J Intensive Care. 2021 Apr 16;9(1):35. doi: 10.1186/s40560-021-00546-8.
Heatstroke 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.
Mildly 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.
The 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.
We 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.
中暑与暴露于高环境温度（AT）和相对湿度（RH）有关，会增加器官损伤或死亡的风险。先前提出的中暑动物模型忽略了相对湿度的影响。因此，我们旨在建立并验证一种考虑相对湿度的中暑动物模型。为了验证我们的模型，我们还研究了补液的效果，并调查了热暴露后肠膜中共转运蛋白的基因表达。
将轻度脱水的成年雄性C57/BL6J小鼠置于相对湿度>99%的三种环境温度条件（37℃、41℃或43℃）下1小时，并用湿球黑球温度（WBGT）进行监测。评估存活率、体重、核心体温、血液参数以及组织学证实的组织损伤，以建立小鼠中暑模型。然后，小鼠在热暴露前后不接受治疗、饮水或口服补液盐（ORS）；使用我们的模型比较随后的器官损伤情况。此后，我们研究了未接受治疗、饮水或ORS的小鼠肠膜中共转运蛋白基因的表达。
暴露于37℃、41℃和43℃环境温度下的小鼠存活率分别为100%、83.3%和0%。根据这一结果，我们排除了43℃。41℃组的小鼠似乎比37℃组的小鼠脱水更严重。41℃组的WBGT>44℃；该组小鼠在热暴露期间核心体温达到41.3±0.08℃，并降至34.0±0.18℃，8小时后恢复到基线水平，呈现出双相热调节反应。41℃组的肝脏、肾脏和肌肉骨骼损伤比其他组更严重。ORS对恢复的影响大于饮水或不治疗。热暴露时给予ORS可增加肠道中共转运蛋白基因的表达，并减少中暑相关损伤。
我们开发了一种考虑环境温度和相对湿度的新型小鼠中暑模型。我们发现，给予ORS可改善循环不足，并通过增加肠道中共转运蛋白基因的表达来减少组织损伤。
