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首页> 外文期刊>Psychosomatic Medicine: Journal of the American Psychosomatic Society >Mechanisms and mediators of psychological stress-induced rise in core temperature.
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Mechanisms and mediators of psychological stress-induced rise in core temperature.

机译：心理压力引起的核心温度升高的机制和媒介。

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OBJECTIVE: Despite numerous case reports on "psychogenic fever," it remains uncertain how psychological stress raises core temperature and whether the rise in core temperature is a real fever or a hyperthermia. This article reviews studies on the psychological stress-induced rise in core temperature (PSRCT) in animals with the aim to facilitate studies on the mechanisms of so-called psychogenic fever in humans. METHODS: To address this question, we reviewed the mechanisms and mediators of the PSRCT and classic conditioning of the fever response in animals. RESULTS: The PSRCT is not due to the increased locomotor activity during stress, and the magnitude of the PSRCT is the same in warm and cold environments, indicating that it is a centrally regulated rise in temperature due to an elevated thermoregulatory "set point." The PSRCT caused by conventional psychological stress models, such as open-field stress, is attenuated by cyclooxygenase inhibitors, which block prostaglandin synthesis. On the other hand, the PSRCT elicited by an "anticipatory anxiety stress" is not inhibited by cyclooxygenase inhibitors but by benzodiazepines and serotonin Type 1A receptor agonists. The febrile response can be conditioned to neutral stimuli after paired presentation with unconditioned stimuli such as injection of lipopolysaccharide, a typical pyrogen. CONCLUSIONS: Most findings indicate that the PSRCT is a fever, a rise in the thermoregulatory set point. The PSRCT may occur through prostaglandin E2-dependent mechanisms and prostaglandin E2-independent, 5-HT-mediated mechanisms. The febrile response can be conditioned. Thus, these mechanisms might be involved in psychogenic fever in humans.
机译：目的：尽管有许多关于“心理发烧”的病例报道，但仍不确定心理压力如何升高核心温度，以及核心温度的升高是真正的发烧还是体温过高。本文综述了有关动物心理应激诱导的核心温度升高（PSRCT）的研究，目的是促进对人类所谓的心理发烧机制的研究。方法：为解决这个问题，我们回顾了PSRCT的机制和介质以及动物发烧反应的经典条件。结果：PSRCT并不是由于在压力作用下运动活动增加而引起的，而在温暖和寒冷的环境中，PSRCT的大小都相同，这表明由于温度调节“设定点”的升高，温度是中央调节的。由传统的心理压力模型（例如开场压力）引起的PSRCT被环加氧酶抑制剂所抑制，后者会阻碍前列腺素的合成。另一方面，由“预期焦虑应激”引起的PSRCT不受环氧合酶抑制剂的抑制，但受到苯二氮卓类和血清素1A型受体激动剂的抑制。与无条件的刺激（如注射脂多糖，一种典型的热原）配对配对后，可将发热反应调节至中性刺激。结论：大多数发现表明PSRCT是发烧，体温调节设定值升高。 PSRCT可能通过前列腺素E2依赖性机制和独立于前列腺素E2的5-HT介导的机制发生。可以调节发热反应。因此，这些机制可能与人类的心理发烧有关。

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