Role of bacterial endotoxins of intestinal origin in rat heat stress mortality

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Abstract
Using unanesthetized rats, the effect on heat stress mortality of endotoxin tolerance or zymosan treatment was determined. 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.degree. C.cntdot.min) was significantly greater (P < 0.001) than that for nontolerant rats (44.03.degree. C.cntdot.min). Rats were significantly (P < 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. Although 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.