MacKenzie M, Hermus A, Wollersheim H, Thien T, Pieters G, Smals A, Binkhorst R, Kloppenborg P
Department of Medicine, University Hospital Nijmegen, The Netherlands.
Arctic Med Res. 1991;Suppl:532-3.
To investigate the thermoregulatory mechanisms underlying poikilothermia in man, we have studied 4 female patients (age 28-37 yr) with poikilothermia, most probably of hypothalamic origin, as well as 4 female volunteers of similar age. In a climatic chamber the participants were subjected to cold stress (16.5 degrees C) and subsequent heat exposure (40 degrees C). In the volunteers cold stress did not influence the rectal temperature; cooling induced a marked shivering response and an immediate peripheral vasoconstriction. Subsequent heat challenge induced a slight rise in the rectal temperature (from 36.3 +/- 0.2 to 37.0 +/- 0.3 degrees C) and a marked sweat secretion in all control subjects. All patients were hypothermic at the start of the experiment. Cooling induced a decrease in the rectal temperature of 0.3-0.9 degrees C. Three patients showed neither peripheral vasoconstriction nor a shivering response to cold stress. In contradistinction to the control subjects, in all patients an afterdrop of the rectal temperature of 0.3-0.5 degrees C was observed once heating of the environment had started; thereafter a progressive rise in core temperature occurred up to 38.5 (38.0) degrees C. In none of the patients sweat secretion was clinically visible. These results reveal that in these patients with poikilothermia the disorder of thermoregulation is accompanied by inadequate cutaneous vasomotor adjustment and disturbed sweat response and likely reduced metabolic response to cold stress.
为了研究人类体温调节障碍的潜在机制，我们对4名体温调节障碍的女性患者（年龄28 - 37岁）进行了研究，她们的体温调节障碍很可能源于下丘脑，同时还研究了4名年龄相仿的女性志愿者。在气候舱中，参与者先接受冷应激（16.5摄氏度），随后接受热暴露（40摄氏度）。在志愿者中，冷应激并未影响直肠温度；降温引发了明显的寒战反应和立即的外周血管收缩。随后的热刺激使所有对照受试者的直肠温度略有升高（从36.3±0.2摄氏度升至37.0±0.3摄氏度），并伴有明显的出汗分泌。所有患者在实验开始时体温过低。降温使直肠温度下降了0.3 - 0.9摄氏度。三名患者对冷应激既未表现出外周血管收缩，也未出现寒战反应。与对照受试者不同的是，一旦环境开始升温，所有患者的直肠温度均出现了0.3 - 0.5摄氏度的体温后降；此后，核心温度逐渐上升至38.5（38.0）摄氏度。在所有患者中均未观察到临床上可见的出汗分泌。这些结果表明，在这些体温调节障碍的患者中，体温调节紊乱伴随着皮肤血管运动调节不足、出汗反应紊乱，并且可能对冷应激的代谢反应降低。
