Time course of endotoxemia and cardiovascular changes in heat-stressed primates.

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.