Long N C, Vander A J, Kunkel S L, Kluger M J
Departments of Physiology, University of Michigan Medical School, Ann Arbor 48109.
Am J Physiol. 1990 Mar;258(3 Pt 2):R591-5. doi: 10.1152/ajpregu.1990.258.3.R591.
Psychological stress (e.g., exposure to a novel environment) causes a rapid rise in body temperature in rats. In this study, we examined the roles of physical activity and the immune cytokine tumor necrosis factor or cachectin (TNF) in this temperature change. The elevation in temperature of rats exposed to cage-switch stress during the day correlated poorly with the increase in activity (r = 0.07; P = 0.84) and, during cage switch at night, correlated negatively (r = 0.64; P = 0.04). TNF was not detected in the plasma or cerebrospinal fluid of rats after exposure to open-field stress. However, the injection of antiserum against TNF 3.5 h before exposure to the stress of being in an open field resulted in a significantly greater hyperthermia than was seen in the control serum-injected rats (1.38 +/- 0.11 vs. 0.79 +/- 0.14 degrees C; P = 0.002). The peak temperature change after cage-switch stress was similarly increased in rats that had been injected with anti-TNF (0.82 +/- 0.08 vs. 0.50 +/- 0.08 degrees C; P = 0.016). This enhanced hyperthermia is similar to the excessively high fever that occurs during the later phase of lipopolysaccharide fever in animals that have been injected with antiserum against TNF. These data support the hypotheses that stress hyperthermia is a true fever and that TNF is an endogenous antipyretic, limiting the magnitude of this fever.
心理应激（如暴露于新环境）会导致大鼠体温迅速升高。在本研究中，我们研究了身体活动以及免疫细胞因子肿瘤坏死因子或恶病质素（TNF）在这种体温变化中的作用。白天经历笼舍转换应激的大鼠体温升高与活动增加的相关性较差（r = 0.07；P = 0.84），而在夜间笼舍转换期间，两者呈负相关（r = 0.64；P = 0.04）。暴露于旷场应激后的大鼠血浆或脑脊液中未检测到TNF。然而，在暴露于旷场应激前3.5小时注射抗TNF抗血清，导致体温显著高于注射对照血清的大鼠（1.38±0.11℃对0.79±0.14℃；P = 0.002）。笼舍转换应激后，注射抗TNF的大鼠体温变化峰值也同样升高（0.82±0.08℃对0.50±0.08℃；P = 0.016）。这种增强的体温过高类似于在注射抗TNF抗血清的动物中，脂多糖发热后期出现的过高热。这些数据支持以下假设：应激性体温过高是一种真正的发热，并且TNF是一种内源性解热物质，可限制这种发热的程度。
