Murazumi K
Department of Physiology, Asahikawa Medical College, Japan.
Hokkaido Igaku Zasshi. 1988 Jan;63(1):85-96.
In order to elucidate the mechanism (S) involved in improved cold tolerance by means of enhanced non-shivering thermogenesis of the repetitively stressed rats, noradrenaline (NA) turnover of brown adipose tissue (BAT) and adrenocortical responses were investigated. (1) NA turnover of BAT in the cold-acclimated rats was greater than that in the resting controls. NA level of BAT in the cold-acclimated rats decreased to about 40% of the control level. It was thus inferred that this lower NA levels was induced by accelerated NA turnover. (2) NA turnover of BAT in the stressed rats after repetitive immobilization stress was higher than that of the non-stressed controls. Therefore, increased sympathetic activity of BAT would be one of the mechanisms of cross adaptation between cold and stress. (3) NA turnovers of BAT in the controls, the cold-acclimated rats and stressed ones were increased by acute cold exposure (-5 degrees C). NA turnovers of BAT in the controls and the stressed rats were increased by acute immobilization stress. (4) Plasma corticoids (corticosterone and deoxycorticosterone) in the cold-acclimated rats were higher than that of controls. Plasma corticoids in the controls, the cold-acclimated rats and stressed ones were increased by acute cold exposure (-5 degrees C, 15 min) and acute immobilization stress (30 min). The extents of increases in plasma corticoids in the stressed rats, but not in the cold-acclimated ones, were greater than those in the controls. It was suggested that repetitive immobilization stress could enhance nonshivering thermogenesis via an enhanced responsiveness of adrenocortical secretion to acute stress and cold. It would be concluded from these results that enhanced responses of corticoid secretion and accelerated sympathetic activity were associated with the establishment of cross adaptation between cold and stress. It was suggested that the extent of participation of these factors was not necessarily the same between the cold-acclimated and the stressed organisms.
为了阐明反复应激大鼠通过增强非寒战产热提高耐寒性所涉及的机制,研究了棕色脂肪组织(BAT)的去甲肾上腺素(NA)周转率和肾上腺皮质反应。(1)冷适应大鼠BAT的NA周转率高于静息对照组。冷适应大鼠BAT的NA水平降至对照水平的约40%。因此推断,这种较低的NA水平是由NA周转率加快所致。(2)反复固定应激后应激大鼠BAT的NA周转率高于非应激对照组。因此,BAT交感神经活动增强将是寒冷与应激之间交叉适应的机制之一。(3)对照组、冷适应大鼠和应激大鼠的BAT的NA周转率因急性冷暴露(-5℃)而增加。对照组和应激大鼠的BAT的NA周转率因急性固定应激而增加。(4)冷适应大鼠的血浆皮质激素(皮质酮和脱氧皮质酮)高于对照组。对照组、冷适应大鼠和应激大鼠的血浆皮质激素因急性冷暴露(-5℃,15分钟)和急性固定应激(30分钟)而增加。应激大鼠而非冷适应大鼠血浆皮质激素的增加程度大于对照组。提示反复固定应激可通过增强肾上腺皮质分泌对急性应激和寒冷的反应性来增强非寒战产热。从这些结果可以得出结论,皮质激素分泌反应增强和交感神经活动加速与寒冷和应激之间交叉适应的建立有关。提示这些因素在冷适应和应激生物体中的参与程度不一定相同。