Department of Pathology, University of Arizona College of Medicine, 1501 North Campbell Avenue, Tucson, Arizona 85724, USA.
Endocrinology. 2010 Mar;151(3):1187-93. doi: 10.1210/en.2009-1112. Epub 2010 Jan 5.
Hot flushes represent a disorder of central thermoregulation characterized by the episodic activation of heat loss mechanisms. Although flushes are associated with estrogen withdrawal, there is little understanding of the effects of estrogen on thermoregulation in any species. It has been proposed that hormone withdrawal increases the sensitivity of hypothalamic neural pathways that control heat dissipation effectors. If so, we predicted that ovariectomized rats without estradiol treatment would activate tail skin vasodilatation (a major heat loss effector) at lower ambient temperatures and thereby lower the thermoneutral zone. The thermoneutral zone, defined as the range of ambient temperatures in which thermoregulation is achieved only by sensible (dry) heat loss, was evaluated based on properties of skin vasomotion. Core and tail skin temperatures were recorded in ovariectomized rats (with and without estradiol-17beta) exposed to ambient temperatures from 13 to 34 C in an environmental chamber. Rats without estradiol exhibited increased skin vasodilatation and a shift in the thermoneutral zone to lower ambient temperatures. Moreover, the ambient temperature threshold for skin vasodilatation was significantly lower in rats without estradiol treatment. At most ambient temperatures, average core temperature was unaffected by estradiol. However, at ambient temperatures of 32.5 C and above, untreated ovariectomized rats exhibited higher core temperatures compared with estradiol-treated rats. Thus, estradiol-17beta treatment enhanced the maintenance of core temperature during heat exposure. These findings support the hypothesis that estrogen withdrawal increases the sensitivity of thermoregulatory neural pathways and modifies the activation of heat loss mechanisms.
热潮代表了一种以散热机制的间歇性激活为特征的中枢体温调节障碍。尽管热潮与雌激素撤退有关,但对于任何物种,雌激素对体温调节的影响知之甚少。有人提出,激素撤退会增加控制散热效应器的下丘脑神经通路的敏感性。如果是这样,我们预测没有雌激素治疗的去卵巢大鼠会在较低的环境温度下激活尾部皮肤血管扩张(主要的散热效应器),从而降低热中性区。热中性区定义为仅通过感觉(干燥)热损失来实现体温调节的环境温度范围,根据皮肤血管运动的特性进行评估。在环境室中,将去卵巢大鼠(有或没有雌二醇-17β)暴露于 13 至 34°C 的环境温度下,记录核心和尾部皮肤温度。没有雌激素的大鼠表现出皮肤血管扩张增加和热中性区向较低环境温度的转移。此外,没有雌激素治疗的大鼠的皮肤血管扩张的环境温度阈值明显较低。在大多数环境温度下,平均核心温度不受雌激素影响。然而,在环境温度为 32.5°C 及以上时,未经处理的去卵巢大鼠的核心温度比接受雌激素治疗的大鼠高。因此,雌二醇-17β治疗增强了在热暴露期间维持核心温度的能力。这些发现支持了这样的假设,即雌激素撤退增加了体温调节神经通路的敏感性,并改变了散热机制的激活。