ACUTE HEAT-STRESS PROTECTS RATS AGAINST ENDOTOXIN-SHOCK
ACUTE HEAT-STRESS PROTECTS RATS AGAINST ENDOTOXIN-SHOCK
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DOI：
10.1152/jappl.1992.73.4.1517
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发表时间：
1992-10-01
影响因子：
3.3
通讯作者：
GISOLFI, CV
中科院分区：
文献类型：
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作者：
RYAN, AJ;FLANAGAN, SW;GISOLFI, CV
本研究的目的是确定1)预先(24小时)热应激是否会使大鼠对细菌脂多糖(LPS)的致死活性产生交叉抗性，以及2)这种获得性抵抗状态是否与热应激事件中的内毒素血症有关。实验分为4组(n=7/组)：1)生理盐水组，2)脂多糖组，3)热应激+生理盐水组，4)热应激+脂多糖组。热应激大鼠暴露于高温(环境温度47-50℃，相对湿度30%)后24小时静脉注射生理盐水或内毒素(大肠杆菌，0111：B4型，20 mg/kg体重)，非热应激大鼠在一天中的同一时间给予生理盐水或内毒素(大肠杆菌，0111：B4型，20 mg/kg体重)，观察存活48小时。热应激生理盐水组和热应激脂多糖处理组的最高核心温度(T(C))和超过T(C)的时间分别为42.7+/-0.1和42.6+/-0.1-C(SE)和44.0+/-2.1和47.9+/-3.7(SE)。给非加温大鼠注射内毒素，致死率为71.4%(5/7)。相反，所有(7/7)大鼠在内毒素治疗前24小时都经历了单一的非致命性热应激事件(P<；0.05)。暴露于42.9+/-0.1-C温度的大鼠(n=6)在热应激后即刻动脉血浆中未检测到内毒素。这些发现表明，急性热应激可以保护大鼠免受内毒素的致死作用。
The purpose of this study was to determine 1) whether prior (24-h) heat stress could render rats cross-resistant to the lethal activity of bacterial lipopolysaccharide (LPS) and 2) whether this acquired state of resistance is associated with endotoxemia during the heat stress event. Four groups (n = 7/group) of rats were examined: 1) saline treated, 2) LPS treated, 3) heat stressed and saline treated, and 4) heat stressed and LPS treated. Saline or LPS (Escherichia coli, serotype 0111:B4, 20 mg/kg body wt) was given intravenously 24 h after exposure to heat (ambient temperature 47-50-degrees-C, relative humidity 30%) for heat-stressed rats and at the same time of day for nonheated rats; survival was monitored for 48 h. Thermal responses were similar (P > 0.05); values for maximum core temperature (T(c)) and time above T(c) of 40-degrees-C were 42.7 +/- 0.1 and 42.6 +/- 0.1-C (SE) and 44.0 +/- 2.1 and 47.9 +/- 3.7 (SE) min for the heat-stressed saline-treated and heat-stressed LPS-treated rats, respectively. Administration of LPS to nonheated rats resulted in 71.4% (5 of 7 rats) lethality. In contrast, all (7 of 7) rats subjected to a single nonlethal heat stress event 24 h before LPS treatment survived (P < 0.05). Endotoxin was not detected in arterial plasma immediately after heat stress in rats (n = 6) exposed to a T(c) of 42.9 +/- 0.1-degrees-C. These findings demonstrate that acute heat stress can protect rats from the lethal activity of LPS.