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AJP - Regulatory, Integrative and Comparative Physiology, Vol 273, Issue 3 858-R863, Copyright © 1997 by American Physiological Society
ARTICLES |
M. J. Kluger, K. Rudolph, D. Soszynski, C. A. Conn, L. R. Leon, W. Kozak, E. S. Wallen and P. L. Moseley
Lovelace Respiratory Research Institute, Albuquerque 87108, USA.
Exposure to heat stress leads to both short-term and long-term effects on morbidity. Male rats were exposed to a high ambient temperature of 40 degrees C, which resulted in biotelemetered core body temperature rising to approximately 42 degrees C. This treatment led to a marked enhancement in lipopolysaccharide (LPS)-induced fever at 24 h after exposure to heat stress. The increase in fever was accompanied by a significant suppression in the circulating concentration of tumor necrosis factor. Heat-shock protein-70 measured in liver was elevated by the heat exposure (but not further elevated by the injection of LPS). An enhanced fever to LPS and other inflammatory stimuli found in heat-stressed human subjects could explain the apparent increase in susceptibility to disease.
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