Gathiram P, Gaffin S L, Brock-Utne J G, Wells M T
Department of Physiology, University of Natal Medical School, Durban, South Africa.
Aviat Space Environ Med. 1987 Nov;58(11):1071-4.
Heat stress causes a marked reduction in splanchnic blood flow in order to compensate for the increased flow to the skin. Splanchnic ischemia causes a leakage of endotoxins from the gut lumen into the portal circulation and, especially in the presence of a compromised reticuloendothelial system, may cause severe systemic endotoxemia. Since many of the pathological features of heat stroke are similar to the shock state produced by LPS, we examined whether heat-stress causes endotoxemia. Five anesthetized monkeys were subjected to an environmental temperature of 41 degrees +/- 0.3 degrees C and relative humidity of 100%, until death. Rectal temperatures were recorded continuously, blood pressure and ECG were recorded at 5-min intervals, and arterial blood samples were taken at 15-30 min intervals. A decline in mean arterial pressure and rapid rise in heart rate occurred at about 42 degrees C. Plasma LPS remained at 0.071 +/- 0.006 ng.ml-1 until a rectal temperature of +/- 42 degrees C. Thereafter, it increased slowly until beyond 43 degrees C when it rose rapidly to 0.347 +/- 0.024 prior to death. Endotoxemia may have been a contributing factor in the pathogenesis of heat stroke. If so, then the use of anti-LPS antibodies may be expected to be beneficial.
热应激会导致内脏血流量显著减少，以补偿流向皮肤的血流量增加。内脏缺血会导致内毒素从肠腔漏入门静脉循环，尤其是在网状内皮系统受损的情况下，可能会导致严重的全身内毒素血症。由于中暑的许多病理特征与脂多糖产生的休克状态相似，我们研究了热应激是否会导致内毒素血症。五只麻醉的猴子置于环境温度为41摄氏度±0.3摄氏度、相对湿度为100%的环境中，直至死亡。连续记录直肠温度，每隔5分钟记录血压和心电图，每隔15 - 30分钟采集动脉血样本。平均动脉压在约42摄氏度时下降，心率迅速上升。血浆脂多糖在直肠温度达到±42摄氏度之前一直保持在0.071±0.006 ng.ml-1。此后，它缓慢上升，直到超过43摄氏度时迅速升至0.347±0.024，直至死亡。内毒素血症可能是中暑发病机制中的一个促成因素。如果是这样，那么使用抗脂多糖抗体可能会有益。
