Hynson J M, Sessler D I, Moayeri A, McGuire J
Department of Anesthesia, University of California, San Francisco, School of Medicine 94143-0648.
Anesthesiology. 1993 Oct;79(4):695-703. doi: 10.1097/00000542-199310000-00010.
Typically, core temperature rapidly decreases after induction of anesthesia, but reaches a stable plateau after several hours. This plateau typically occurs in conjunction with the onset of thermoregulatory vasoconstriction. Decreased heat loss, caused by vasoconstriction, may not be sufficient to establish thermal steady state without a concomitant increase in heat production. Accordingly, the authors tested the hypothesis that nonshivering thermogenesis contributes to thermal steady state during anesthesia. Rewarming from hypothermia is often associated with an afterdrop (a further reduction in core temperature, despite cutaneous warming). Because total body heat content increases during cutaneous warming, heat storage during afterdrop must reflect increased temperature and heat content of the peripheral tissue mass. Thermal balance was measured during rewarming to estimate the thermal capacity of the peripheral tissues.
Five volunteers were anesthetized with isoflurane and paralyzed with vecuronium. Oxygen consumption was measured during cooling to a core temperature at least 1 degree C less than that which triggered vasoconstriction. Volunteers were subsequently rewarmed using a circulating-water blanket and forced-air warmer. Oxygen consumption and cutaneous heat flux were measured to assess thermal balance and peripheral tissue heat storage during rewarming.
The core temperature threshold for vasoconstriction was 35.2 +/- 0.8 degrees C. Oxygen consumption decreased 9 +/- 5%/degrees C during active cooling before vasoconstriction and 9 +/- 3%/degrees C after vasoconstriction. After the start of rewarming, core temperature continued to decrease for an additional 32 +/- 8 min. The magnitude of this afterdrop was 0.6 +/- 0.1 degree C. Peripheral tissue heat storage measured from the start of rewarming until the first net increase in core temperature was 144 +/- 60 kcal, which approximately equals 2 h of resting metabolic heat production.
The authors concluded that nonshivering thermogenesis is not an important thermoregulatory response in adults anesthetized with isoflurane. Afterdrop and delayed core temperature recovery during rewarming reflect the large heat storage capacity of peripheral tissues.
通常,麻醉诱导后核心体温会迅速下降,但数小时后会达到一个稳定的平台期。这个平台期通常与体温调节性血管收缩的开始同时出现。血管收缩导致的热量散失减少,若没有伴随产热增加,可能不足以建立热稳态。因此,作者检验了如下假设:非寒战产热有助于麻醉期间的热稳态。从低温复温常常与体温后降(尽管皮肤升温,但核心体温进一步降低)相关。因为皮肤升温期间全身热量含量增加,体温后降期间的热量储存必定反映了外周组织质量的温度和热量含量增加。复温期间测量热平衡以估计外周组织的热容量。
五名志愿者用异氟烷麻醉并用维库溴铵使其麻痹。在冷却至比触发血管收缩的核心体温至少低1℃的过程中测量耗氧量。随后使用循环水毯和强制空气加热器使志愿者复温。测量耗氧量和皮肤热通量以评估复温期间的热平衡和外周组织热量储存。
血管收缩的核心体温阈值为35.2±0.8℃。在血管收缩前主动冷却期间耗氧量每℃下降9±5%,血管收缩后下降9±3%。复温开始后,核心体温又持续下降了32±8分钟。这个体温后降的幅度为0.6±0.1℃。从复温开始到核心体温首次净增加时测量的外周组织热量储存为144±60千卡,这大约相当于2小时的静息代谢产热。
作者得出结论,非寒战产热在接受异氟烷麻醉的成人中不是重要的体温调节反应。复温期间的体温后降和核心体温延迟恢复反映了外周组织的巨大热量储存能力。