Kurz A, Sessler D I, Christensen R, Clough D, Plattner O, Xiong J
Acta Anaesthesiol Scand Suppl. 1996;109:30-3.
Heat transfer between the core and its environment in normothermic and slightly hypothermic situations is determined largely by the influence of vasomotion on convection. Tonic vasoconstriction, the normal barrier to heat loss from the core, is impaired upon induction of anesthesia. The resulting dilation of the arteriovenous shunts leads to redistribution of heat from the core to the periphery, diminishing the temperature gradient between the two compartments. With reemergence of thermoregulatory vasoconstriction at core temperatures near 34 degrees C, the core and the periphery are again separated, with metabolic heat being largely constrained to the core. Under normal conditions of mild thermal stress, thermoregulatory vasoconstriction is thus able to protect core temperature by reducing cutaneous heat transfer and functionally isolating the peripheral and core thermal compartments. Consequently, anesthetic-induced alterations in vasomotor tone is one of the major factors influencing core temperature in patients who are not actively cooled or warmed. In contrast, thermoregulatory tone is insufficient to prevent core temperature perturbations in patients undergoing vigorous cutaneous cooling or warming.
在正常体温和轻度低温情况下,核心体温与其周围环境之间的热传递在很大程度上取决于血管运动对对流的影响。紧张性血管收缩是核心体温散热的正常屏障,在麻醉诱导时会受到损害。由此导致的动静脉分流扩张会使热量从核心体温重新分布到外周,减小两个腔室之间的温度梯度。当核心体温接近34摄氏度时,体温调节性血管收缩再次出现,核心体温和外周体温再次分离,代谢产生的热量主要被限制在核心体温。因此,在轻度热应激的正常情况下,体温调节性血管收缩能够通过减少皮肤热传递并在功能上隔离外周和核心体温腔室来保护核心体温。因此,麻醉引起的血管运动张力改变是影响未进行主动降温或升温患者核心体温的主要因素之一。相比之下,在进行剧烈皮肤降温或升温的患者中,体温调节张力不足以防止核心体温波动。