Banet M
Institute for Normal and Pathological Physiology, Philipps University, Marburg, Federal Republic of Germany.
J Appl Physiol (1985). 1988 Mar;64(3):1076-8. doi: 10.1152/jappl.1988.64.3.1076.
To study the mechanism of action of physical antipyresis, core temperature was measured in two groups of rats in which heat loss was increased by cold exposure and by cooling an inferior cava heat exchanger, respectively, both before and after infection with Salmonella enteritidis. Cold exposure did not influence core temperature. On the other hand, cooling the heat exchanger caused a fall in core temperature of approximately 0.7 degree C, to 37 degrees C in normothermia and to 38.5 degrees C 24 h after the infection. These lower core temperatures were then regulated against any further increase in heat loss until the thermoregulatory metabolic capacity of the animals was exhausted and a hypothermia developed. It is concluded that in infectious fever the threshold temperature of shivering increases as much as core temperature. Furthermore it is suggested that physical antipyresis, such as sponging with tepid water, induces a moderate but regulated fall in temperature to about the threshold of shivering and that its efficacy may increase with ambient temperature.
为研究物理退热的作用机制，分别通过冷暴露和冷却下腔静脉热交换器增加两组大鼠的散热，在肠炎沙门氏菌感染前后测量其核心体温。冷暴露不影响核心体温。另一方面，冷却热交换器导致核心体温下降约0.7摄氏度，在正常体温下降至37摄氏度，感染后24小时降至38.5摄氏度。这些较低的核心体温随后被调节以防止散热进一步增加，直到动物的体温调节代谢能力耗尽并出现体温过低。得出的结论是，在感染性发热中，寒战的阈值温度与核心体温升高幅度相同。此外，有人提出，物理退热，如用温水擦拭，会使体温适度但有调节地下降至约寒战阈值，其效果可能会随环境温度升高而增强。
