TISSUE-SPECIFIC HSP70 RESPONSE IN ANIMALS UNDERGOING HEAT-STRESS
TISSUE-SPECIFIC HSP70 RESPONSE IN ANIMALS UNDERGOING HEAT-STRESS
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DOI：
10.1152/ajpregu.1995.268.1.r28
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发表时间：
1995-01-01
影响因子：
2.8
通讯作者：
MOSELEY, PL
中科院分区：
文献类型：
--
作者：
FLANAGAN, SW;RYAN, AJ;MOSELEY, PL
中暑是一种多系统疾病，可导致死亡。增加储热速率的活动使生物体易于受到热损伤。使用72-kDa热休克蛋白（HSP 72）作为热损伤的标志物，我们确定1）哪些器官在高温后合成HSP，以及2）高加热速率（HHR）是否比低加热速率（LHR）导致更多的HSP 72。将大鼠分配到对照组、HHR（0.166 ℃/min）组或LHR（0.045 ℃/min）组。当结肠温度（T-c）达到42 ℃时，热暴露结束。与LHR动物相比，HHR动物在热和热负荷中的总时间（测量为动物保持T-c > 40.4摄氏度的时间）显著较低。高温导致肝脏、小肠和肾脏中HSP 72的组织特异性增加，但在大脑或四头肌中没有。此外，与LHR组动物相比，HHR动物肝脏中HSP 72的积累显着增加。因此，HSP 72的合成在高生理温度下是组织特异性的，并且可以识别对早期热损伤敏感的关键靶组织。
Heatstroke is a multisystem disorder that can result in death. Activities that increase the rate of heat storage predispose an organism to thermal injury. Using a 72-kDa heat shock protein (HSP72) as a marker of thermal injury, we determined 1) which organs synthesize HSP in animals after hyperthermia and 2) whether a high heating rate (HHR) resulted in more HSP72 than a low heating rate (LHR). Rats were assigned to either control, HHR (0.166 degrees C/min), or LHR (0.045 degrees C/min) groups. Heat exposure ended when colonic temperature (T-c) reached 42 degrees C. Total time in the heat and thermal load (measured as the time an animal maintained a T-c > 40.4 degrees C) were significantly lower in HHR compared with LHR animals. Hyperthermia resulted in a tissue-specific increase in HSP72 in the liver, small intestine, and kidney, but not in the brain or quadriceps muscles. In addition, HHR animals showed significantly greater accumulation of HSP72 in the liver compared with animals in the LHR group. Thus HSP72 synthesis is tissue specific at high physiological temperatures and may identify a critical target tissue susceptible to early thermal damage.