Mansell P I, Fellows I W, MacDonald I A, Allison S P
Queen's Medical Centre, Nottingham.
Q J Med. 1990 Aug;76(280):817-29.
Previous studies in infants and in the elderly have shown that a low body weight is associated with a defect in thermoregulation and an increased risk of hypothermia. In the present study, thermoregulatory responses to a cooling stimulus were measured in 10 young and middle-aged patients who lost at least 10 per cent of their body weight during illness. Investigations were performed before and after restoration of body weight (mean weight gain 7.2 kg, SE 1.2 kg, p less than 0.001). The cooling stimulus was provided by a special suit perfused with water at 28 degrees C and then at 23 degrees C. Before weight gain, there was no increase in metabolic rate in response to cooling, despite a fall in core temperature. Following weight gain, the thermogenic response to cooling was restored towards normal. Peripheral vasoconstriction, the principal mechanism for heat conservation, was similar before and after weight gain. The thermogenic response to an infusion of adrenaline (25 ng/kg/min) was not abolished by weight loss, suggesting that the defect in cold-induced thermogenesis following weight loss is due to a change in central control mechanisms of thermoregulation, and not to tissue unresponsiveness. The phenomenon of abnormal thermoregulation following weight loss and the return to normal with subsequent weight gain may be clinically important, particularly in the elderly, since quite small falls in core temperature may impair both neuromuscular coordination and cerebral function.
先前针对婴儿和老年人的研究表明，低体重与体温调节缺陷以及体温过低风险增加有关。在本研究中，对10名在患病期间体重至少减轻10%的中青年患者进行了对降温刺激的体温调节反应测量。在体重恢复前后进行了调查（平均体重增加7.2千克，标准误1.2千克，p小于0.001）。降温刺激由一套特殊的套装提供，先灌注28摄氏度的水，然后灌注23摄氏度的水。在体重增加前，尽管核心体温下降，但对降温的代谢率没有增加。体重增加后，对降温的产热反应恢复正常。外周血管收缩作为保存热量的主要机制，在体重增加前后相似。体重减轻并未消除对肾上腺素输注（25纳克/千克/分钟）的产热反应，这表明体重减轻后冷诱导产热的缺陷是由于体温调节中枢控制机制的改变，而非组织无反应性。体重减轻后体温调节异常以及随后体重增加后恢复正常的现象可能具有临床重要性，尤其是在老年人中，因为核心体温相当小的下降可能会损害神经肌肉协调和脑功能。
