热打击后小鼠肺和脑组织病理学的改变  

Study on the pathological changes of the lung and brain in mice during heat stress

作　　者：刘志锋 唐柚青 徐秋林 童华生 郭进强[2] 苏磊 

机构地区：[1]广州州军区广州州总医院ICU,广州510010 [2]南方医科大学公共卫生与热带医学学院仿真气候室

出　　处：《中华急诊医学杂志》2011年第6期623-626,共4页Chinese Journal of Emergency Medicine

基　　金：中国博士后科学基金

摘　　要：目的制备小鼠热打击模型，研究热打击和复温治疗过程中动物肺和脑组织的病理形态学改变。方法BALB／c小鼠随机（随机数字法）分为对照组和热打击组，对照组动物始终置于（25±O．5）℃，湿度35±5％环境下，热打击组置于仿真高温气候舱内，舱内温度（35．5±0．5）℃，相对湿度（60±5）％，记录小鼠直肠温度（Tc），并按Tc分为39℃、40℃、41℃、42℃组，分别于Tc达到41℃后移置（25-t-0．5）℃，相对湿度（35±5）％环境下复温12h组和24h组和达到42℃后移置常温复温6h组（n=6）。分离动物肺和脑组织行HE染色，显微镜下观察并照相。结果动物对热打击的Tc变化均一，低程度的热打击即可使肺部发生明显病理改变，进一步的热打击表现为进行性加重的间质血管显著扩张充血，大量肺泡腔出血，部分肺泡上皮细胞脱落，肺泡结构模糊不清，而复温则可以使病变明显减轻。脑组织在低程度的热打击时仅表现为轻度的脑水肿，随着打击程度的加重，除了脑水肿加重外，还渐进性出现神经元细胞变性坏死。在体温达到41℃后复温则病变有所减轻，而体温达到42℃后再复温病变进一步加重。结论肺和脑对热打击和复温的病理改变表现出各自特征性改变，并且同复温的时机和时间有着一定的关系，此为理解中暑发生发展至多脏器功能障碍综合征（MODS）的发病机制提供了实验基础。Objective To prepare mouse model with heat stress and determine its pathological changes of the lung and brain during heat stress. Methods BALB/c mouse were randomly （ random number） divided into two groups, control group and heat stress group. The animals in the control group were shamheated at a temperature of （25±0.5 ） ℃ and humidity of （ 35±5 ） %. The animals of heat stress group were placed in a prewarmed incubator maintained at （35.5 ±0.5 ） ℃ and relative humidity of （60 ± 5 ） %. Rectal temperature （Tc） was monitored, and when Tc respectively reached 39 ℃, 40 ℃, 41 ℃ and 42 ℃, those study animals were killed. The other animals were removed from the incubator and allowed to cool at an ambient temperature of （25 ± 0.5 ）℃ and humidity of （35±5 ）%, respectirvely for 12 and 24 hrs when Tc reached 41 ℃, and for 6 hrs when Tc reached 42 ℃. The lung and brain of all the animals were isolated. Hematoxylin and eosin stain and light microscope were used to detect their pathological changes. Results All the animals displayed uniform response to the heat stress. Low degree of heat stress could induced obviously pathological changes of the lung, progressively greater damage to lung with further congestion of lung matrix, asystematic hemorrhage of alveolar space, abscission of alveolar epithelial cell and disappear of pulmonary alveolus tissue structure were detected with the rise of Tc to 42 ℃. However, absorption of congestion and hemorrhage and recovery of pulmonary alveolus tissue structure could also be seen with cooling at ambient temperature. With low degree of heat stress, the brain only showed moderate edema. Neuronal denaturation and necrosis were detected when Tc reached to 42 ℃. Interestingly, the lesions of brain further aggravated even through cooling treatment after Tc reached to 42 ℃, but recovery could been observed after cooling treatment followed with Tc of 41℃. Conclusions The pathological changes of the lung and brain showed distinctive l

关 键 词：热打击 中暑 肺 脑 病理改变 小鼠 多脏器功能障碍 降温治疗 

分 类 号：R363[医药卫生—病理学]