Belani K, Sessler D I, Sessler A M, Schroeder M, McGuire J, Merrifield B, Washington D E, Moayeri A
University of Minnesota, Minneapolis.
Anesthesiology. 1993 May;78(5):856-63. doi: 10.1097/00000542-199305000-00008.
Sufficient hypothermia during anesthesia provokes thermoregulatory responses, but the clinical significance of these responses remains unknown. Nonshivering thermogenesis does not increase metabolic heat production in anesthetized adults. Vasoconstriction reduces cutaneous heat loss, but the initial decrease appears insufficient to cause a thermal steady state (heat production equaling heat loss). Accordingly, the authors tested the hypotheses that: 1) thermoregulatory vasoconstriction prevents further core hypothermia; and 2) the resulting stable core temperature is not a thermal steady state, but, instead, is accompanied for several hours by a continued reduction in body heat content.
Six healthy volunteers were anesthetized with isoflurane (0.8%) and paralyzed with vecuronium. Core hypothermia was induced by fan cooling, and continued for 3 h after vasoconstriction in the legs was detected. Leg heat content was calculated from six needle thermocouples and skin temperature, by integrating the resulting parabolic regression over volume.
Core temperature decreased 1.0 +/- 0.2 degrees C in the 1 h before vasoconstriction, but only 0.4 +/- 0.3 degrees C in the subsequent 3 h. This temperature decrease, evenly distributed throughout the body, would reduce leg heat content 10 kcal. However, measured leg heat content decreased 49 +/- 18 kcal in the 3 h after vasoconstriction.
These data thus indicate that thermoregulatory vasoconstriction produces a clinically important reduction in the rate of core cooling. This core temperature plateau resulted, at least in part, from sequestration of metabolic heat to the core which allowed core temperature to remain nearly constant, despite a continually decreasing body heat content.
麻醉期间足够的低温会引发体温调节反应,但其临床意义尚不清楚。在麻醉的成年人中,非寒战产热不会增加代谢产热。血管收缩可减少皮肤散热,但最初的减少似乎不足以导致热稳态(产热等于散热)。因此,作者检验了以下假设:1)体温调节性血管收缩可防止核心体温进一步降低;2)由此产生的稳定核心体温不是热稳态,而是在数小时内伴随着身体热量含量的持续降低。
6名健康志愿者接受异氟烷(0.8%)麻醉并用维库溴铵使其麻痹。通过风扇冷却诱导核心体温降低,并在检测到腿部血管收缩后持续3小时。通过将六个针式热电偶和皮肤温度的抛物线回归积分计算腿部热量含量。
在血管收缩前1小时,核心体温下降1.0±0.2℃,但在随后的3小时内仅下降0.4±0.3℃。这种全身均匀分布的体温下降会使腿部热量含量减少10千卡。然而,在血管收缩后的3小时内,测量到的腿部热量含量下降了49±18千卡。
这些数据表明,体温调节性血管收缩可使核心体温下降速率在临床上显著降低。这种核心体温平台期至少部分是由于代谢热向核心的隔离,使得核心体温尽管身体热量含量持续下降仍能保持几乎恒定。