Stoner H B
Br J Exp Pathol. 1969 Apr;50(2):125-38.
The effect of changes in environmental temperature (10-33°) on the rate of O consumption of rats injured by hind-limb ischaemia or scalding has been investigated during the first few hours after injury. In the thermoneutral zone O consumption was not inhibited by trauma unless the injury proved fatal and even then O consumption was maintained at the normal rate until just before death. The critical temperature was lowered by trauma. The depression of this point increased with the severity of the injury. Within this new extended thermoneutral range the O consumption by the injured rats fell to the basal rate of the controls and remained there, only declining further in the terminal stages. At environmental temperatures below the new critical temperature trauma inhibited O consumption but a direct correlation with the environmental temperature was retained. The regression line for O consumption on environmental temperature was moved to the left without altering the slope, the separation from the controls depending on the severity of the injury. Trauma impaired thermoregulation in the rat but it was not possible to identify the site of interference with the mechanism.
研究了环境温度变化(10 - 33°C)对后肢缺血或烫伤致伤大鼠伤后最初数小时耗氧量的影响。在热中性区,除非损伤致命,否则创伤不会抑制耗氧量,即便如此,耗氧量在死亡前一直维持在正常水平。创伤使临界温度降低。该温度点的降低程度随损伤严重程度增加而增大。在这个新的扩展热中性范围内,受伤大鼠的耗氧量降至对照组的基础水平并维持在该水平,仅在终末期进一步下降。在环境温度低于新的临界温度时,创伤抑制耗氧量,但与环境温度仍保持直接相关性。耗氧量与环境温度的回归线向左移动但斜率不变,与对照组的差异取决于损伤的严重程度。创伤损害了大鼠的体温调节,但无法确定干扰该机制的部位。