Horowitz M
Division of Physiology, Hadassah School of Dental Medicine, Hebrew University, Jerusalem, Israel.
J Basic Clin Physiol Pharmacol. 1990 Jan-Dec;1(1-4):267-76. doi: 10.1515/jbcpp.1990.1.1-4.267.
The state of body hydration has a marked effect on thermoregulation during heat stress. Heat stressed hypohydrated mammals reduce evaporative cooling and metabolic rate, and allow their body temperature to rise. This outcome is not a failure in thermoregulation, but readjustment, leading to improved physical avenues for heat dissipation and water conservation. The modulation of the thermoregulatory system is mostly central. This is exhibited by decreased sensitivity of the thermoregulatory integration center and by an upward shift of temperature thresholds for heat dissipation activities. New evidence suggests alterations in effector organs as well. In the euhydrated body, hyperosmolarity and hypovolemia, the consequences of hypohydration, via activation of osmoreceptors and low pressure baroreceptors, induce the same thermoregulatory responses as hypohydration does. Single unit studies on hypothalamic slices provide a neuronal basis for osmoregulation-thermoregulation interaction. The possible role of arginine vasopressin (AVP) as a central modulator in this interaction is discussed.
身体水合状态对热应激期间的体温调节有显著影响。热应激状态下水分不足的哺乳动物会减少蒸发散热和代谢率，并使体温升高。这一结果并非体温调节失败，而是一种重新调整，从而导致改善散热和节水的生理途径。体温调节系统的调节主要发生在中枢。这表现为体温调节整合中心的敏感性降低以及散热活动温度阈值的上移。新证据表明效应器官也会发生改变。在水分充足的机体中，高渗和血容量不足（水分不足的后果）通过激活渗透压感受器和低压压力感受器，会引发与水分不足相同的体温调节反应。对下丘脑切片的单单位研究为渗透调节 - 体温调节相互作用提供了神经元基础。本文讨论了精氨酸加压素（AVP）作为这种相互作用的中枢调节剂的可能作用。
