Using unanesthetized rats, the effect on heat stress mortality of endotoxin tolerance or
zymosan treatment was determined. In addition, the incidence of invasion by gram-negative bacteria and their
endotoxins was studied to evaluate the role of gut-derived bacterial
endotoxins after heat stress. Endotoxin tolerance resulted in heat stress resistance. The estimated mean total thermal area, which induced an LD50 in
endotoxin-tolerant rats (61.85 degrees C . min) was significantly greater (P less than 0.001) than that for non-tolerant rats (44.03 degrees C . min). Rats were significantly (P less than 0.005) more sensitive to
endotoxin after
zymosan treatment, but this treatment did not alter the heat stress mortality rate. The Limulus
amoebocyte lysate test indicated that
endotoxemia did not occur as a result of heat stress. Though a significantly increased incidence of high gram-negative bacterial count in the duodenum was noted, extraintestinal invasion was not found. It was concluded that resistance to heat stress may not be due to protection from gut-derived bacterial
endotoxins, but resistance may possibly be associated with the ability of endotoxin tolerance to protect from
shock syndromes. Thus bacterial
endotoxins of intestinal origin did not appear to have a significant role in rat heat stress mortality.