MacKenzie M A, Hermus A R, Wollersheim H C, Binkhorst R A, Pieters G F
Department of Medicine, University Hospital Nijmegen, The Netherlands.
Q J Med. 1993 Mar;86(3):205-13.
The pathophysiology of afterdrop of core temperature during rewarming in patients with induced or accidental hypothermia remains controversial. We studied the effect of cooling and rewarming in four female patients with acquired poikilothermia and in four normal females. Exposure to cold air (16.5 degrees C) induced shivering and adequate vasoconstriction in normal individuals, without a fall in rectal temperature (Tr; 36.3 +/- 0.2 degrees C [mean +/- SD]); subsequent heating (40 degrees C) induced a rise in Tr to 37.0 +/- 0.3 degrees C and generalized sweating. The four patients all had spontaneous hypothermia (Tr 34.1 +/- 0.9 degrees C) before cooling. Tr decreased by 0.3-0.9 degrees C during cold exposure, and a marked afterdrop of Tr (0.3-0.5 degrees C) occurred during rewarming: this did not occur in normal individuals. Cooling failed to induce shivering and vasoconstriction in three patients. No patient showed visible sweating during heating despite a Tr of up to 38.0-38.5 degrees C and skin temperature of up to 37.7-38.5 degrees C. The basal metabolic rate was decreased by 71-82% in all patients during steady-state hypothermia and remained lowered during normothermia in two patients. We conclude that during hypothermia three of the four patients showed severe disorders of peripheral vasomotor function and shivering response. These data provide evidence for thermal conduction as the major mechanism of afterdrop during hypothermia.
诱导性或意外性体温过低患者复温过程中核心体温后降的病理生理学仍存在争议。我们研究了四名获得性变温症女性患者和四名正常女性的降温及复温效果。正常个体暴露于冷空气(16.5摄氏度)会引发寒战和适当的血管收缩,直肠温度(Tr;36.3±0.2摄氏度[平均值±标准差])无下降;随后加热(40摄氏度)会使Tr升至37.0±0.3摄氏度并出现全身出汗。四名患者在降温前均有自发性体温过低(Tr 34.1±0.9摄氏度)。在冷暴露期间Tr下降了0.3 - 0.9摄氏度,复温期间出现了明显的Tr后降(0.3 - 0.5摄氏度):正常个体未出现这种情况。三名患者在降温时未能引发寒战和血管收缩。尽管Tr高达38.0 - 38.5摄氏度且皮肤温度高达37.7 - 38.5摄氏度,但没有患者在加热期间出现明显出汗。所有患者在体温过低稳态期间基础代谢率降低了71 - 82%,两名患者在体温正常期间仍保持较低水平。我们得出结论,在体温过低期间,四名患者中有三名表现出严重的外周血管运动功能和寒战反应障碍。这些数据为热传导是体温过低期间后降的主要机制提供了证据。