Plattner O, Semsroth M, Sessler D I, Papousek A, Klasen C, Wagner O
Department of Anesthesia, University of California, San Francisco 94143-0648, USA.
Anesthesiology. 1997 Apr;86(4):772-7. doi: 10.1097/00000542-199704000-00006.
Sweating, vasoconstriction, and shivering have been observed during general anesthesia. Among these, vasoconstriction is especially important because-once triggered-it minimizes further hypothermia. Surprisingly, the core-temperature plateau associated with vasoconstriction appears to preserve core temperature better in infants and children than adults. This observation suggests that vasoconstriction in anesthetized infants may be accompanied by hypermetabolism. Consistent with this theory, unanesthetized infants rely on nonshivering thermogenesis to double heat production when vasoconstriction alone is insufficient. Accordingly, the authors tested the hypothesis that intraoperative core hypothermia triggers nonshivering thermogenesis in infants.
With Ethics Committee approval and written parental consent, the authors studied six infants undergoing abdominal surgery. All were aged 1 day to 9 months and weighed 2.4-9 kg. Anesthesia was maintained with propofol and fentanyl. The infants were mechanically ventilated and allowed to cool passively until core (distal esophageal) temperatures reached 34-34.5 degrees C. Oxygen consumption-the authors' index of metabolic rate-was recorded throughout cooling. Because nonshivering thermogenesis triples circulating norepinephrine concentrations, arterial blood was analyzed for plasma catecholamines at approximately 0.5 degree C intervals. Thermoregulatory vasoconstriction was evaluated using forearm-fingertip, skin-surface gradients, with gradients exceeding 4 degrees C, indicating intense vasoconstriction. The patients were subsequently rapidly rewarmed to 37 degrees C. Regression analysis was used to correlate changes in oxygen consumption and plasma catecholamine concentrations with core temperature.
All patients were vasoconstricted by the time core temperature reached 36 degrees C. Further reduction in core temperature to 34-34.5 degrees C did not increase oxygen consumption. Instead, oxygen consumption decreased linearly. Hypothermia also failed to increase plasma catecholamine concentrations.
Even at core temperatures approximately 2 degrees C below the vasoconstriction threshold, there was no evidence of nonshivering thermogenesis. This finding is surprising because all other major thermoregulatory responses have been detected during anesthesia. Infants and children thus appear similar to adults in being unable to increase metabolic rate in response to mild intraoperative hypothermia.
全身麻醉期间可观察到出汗、血管收缩和寒战。其中，血管收缩尤为重要，因为一旦触发，它能将进一步的体温过低降至最低程度。令人惊讶的是，与血管收缩相关的核心体温平台期在婴儿和儿童中似乎比成人能更好地维持核心体温。这一观察结果表明，麻醉状态下婴儿的血管收缩可能伴有代谢亢进。与该理论一致的是，未麻醉的婴儿在仅靠血管收缩不足以维持体温时，会依靠非寒战产热使产热增加一倍。因此，作者检验了术中核心体温过低会触发婴儿非寒战产热这一假设。
经伦理委员会批准并获得家长书面同意后，作者研究了6例接受腹部手术的婴儿。所有婴儿年龄在1天至9个月之间，体重2.4 - 9千克。采用丙泊酚和芬太尼维持麻醉。婴儿接受机械通气，并被动降温，直至核心（食管远端）温度达到34 - 34.5摄氏度。在整个降温过程中记录耗氧量（作者用于衡量代谢率的指标）。由于非寒战产热会使循环去甲肾上腺素浓度增加两倍，因此每隔约0.5摄氏度分析动脉血中的血浆儿茶酚胺。使用前臂 - 指尖皮肤表面梯度评估体温调节性血管收缩，梯度超过4摄氏度表明强烈的血管收缩。随后将患者迅速复温至37摄氏度。采用回归分析来关联耗氧量和血浆儿茶酚胺浓度的变化与核心体温。
当核心体温降至36摄氏度时，所有患者均出现血管收缩。核心体温进一步降至34 - 34.5摄氏度并未增加耗氧量。相反，耗氧量呈线性下降。体温过低也未能增加血浆儿茶酚胺浓度。
即使在核心体温比血管收缩阈值低约2摄氏度时，也没有非寒战产热的证据。这一发现令人惊讶，因为在麻醉期间已检测到所有其他主要的体温调节反应。因此，婴儿和儿童在无法因术中轻度体温过低而增加代谢率方面似乎与成人相似。
