论文部分内容阅读
目的研究热射病呼吸衰竭的发生机制。方法在热应激的家兔,观察了热射病的呼吸和循环功能变化。结果呼吸功能由加速向减慢的转折比循环功能的转折发生早,呼吸衰竭似乎不是继发于循环衰竭。因为急性死亡动物的肺损伤不严重,也无呼吸肌疲劳的征象,所以呼吸衰竭也不是由于外周呼吸器官损伤或功能障碍所致。尽管体温持续上升,降低低位脑干的局部温度,可以延后呼吸衰竭的发生和延长动物的存活时间。结论呼吸中枢的损伤可能在呼吸衰竭发生中起重要作用
Aim To study the mechanism of respiratory failure due to heat stroke. Methods In rabbits with heat stress, the changes of respiration and circulatory function were observed. Results The transition from accelerated to slowed breathing occurred earlier than the turning point in circulatory function, and respiratory failure did not appear to be secondary to circulatory failure. Because acute death animals have less severe lung injury and no signs of respiratory muscle fatigue, respiratory failure is not due to peripheral respiratory injury or dysfunction. Although body temperature continues to rise, lowering the local temperature of the lower brain stem can delay the onset of respiratory failure and prolong the survival of the animal. Conclusion The respiratory center injury may play an important role in the occurrence of respiratory failure