Bernheim H A, Block L H, Atkins E
Ann Intern Med. 1979 Aug;91(2):261-70. doi: 10.7326/0003-4819-91-2-261.
Fever appears to have evolved in vertebrate hosts as an adaptive mechanism for controlling infection. This phenomenon is produced by certain exogenous (largely microbial) stimuli that activated bone-marrow-derived phagocytes to release a fever-inducing hormone (endogenous pyrogen). Endogenous pyrogen, in turn, circulates to the thermoregulatory center of the brain (preoptic area of the anterior hypothalamus) where it causes an elevation in the "set-point" for normal body temperature. Warm blooded animals produced fever by increasing heat production (through shivering) or reducing heat loss (by peripheral vasoconstriction), whereas cold blooded animals do so only by behavioral mechanisms (seeking a warmer environment). This paper discusses current concepts that involve the mechanism of endogenous pyrogen production, the role of central transmittors, and the probable function of fever in combating disease.
发热似乎是脊椎动物宿主进化出的一种控制感染的适应性机制。这种现象是由某些外源性(主要是微生物)刺激产生的,这些刺激激活了骨髓来源的吞噬细胞,使其释放一种发热诱导激素(内源性致热原)。内源性致热原继而循环至大脑的体温调节中枢(下丘脑前部视前区),在那里它会导致正常体温的“调定点”升高。温血动物通过增加产热(通过颤抖)或减少散热(通过外周血管收缩)来产生发热,而冷血动物仅通过行为机制(寻找更温暖的环境)来产生发热。本文讨论了涉及内源性致热原产生机制、中枢递质的作用以及发热在对抗疾病中可能的功能的当前概念。