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Am J Physiol Gastrointest Liver Physiol 276: G1195-G1203, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 5, G1195-G1203, May 1999

Splanchnic tissues undergo hypoxic stress during whole body hyperthermia

David M. Hall1,2, Kirk R. Baumgardner3, Terry D. Oberley4, and Carl V. Gisolfi1

1 Department of Exercise Science and 2 The Free Radical Research Institute, The University of Iowa, Iowa City, Iowa 52242; 3 Department of Cariology, Restorative Sciences, and Endodontics, The University of Michigan, Ann Arbor, Michigan 48109-1078; and 4 Department of Pathology, William H. Middleton Memorial Veterans Affairs Hospital, Madison, Wisconsin 53705

Exposure of conscious animals to environmental heat stress increases portal venous radical content. The nature of the observed heat stress-inducible radical molecules suggests that hyperthermia produces cellular hypoxic stress in liver and intestine. To investigate this hypothesis, conscious rats bearing in-dwelling portal venous and femoral artery catheters were exposed to normothermic or hyperthermic conditions. Blood gas levels were monitored during heat stress and for 24 h following heat exposure. Hyperthermia significantly increased arterial O2 saturation, splanchnic arterial-venous O2 difference, and venous PCO2, while decreasing venous O2 saturation and venous pH. One hour after heat exposure, liver glycogen levels were decreased ~20%. Two hours after heat exposure, the splanchnic arterial-venous O2 difference remained elevated in heat-stressed animals despite normal Tc. A second group of rats was exposed to similar conditions while receiving intra-arterial injections of the hypoxic cell marker [3H]misonidazole. Liver and intestine were biopsied, and [3H]misonidazole content was quantified. Heat stress increased tissue [3H]misonidazole retention 80% in the liver and 29% in the small intestine. Cellular [3H]misonidazole levels were significantly elevated in intestinal epithelial cells and liver zone 2 and 3 hepatocytes and Kupffer cells. This effect was most prominent in the proximal small intestine and small liver lobi. These data provide evidence that hyperthermia produces cellular hypoxia and metabolic stress in splanchnic tissues and suggest that cellular metabolic stress may contribute to radical generation during heat stress.

heat stress; free radical; reactive oxygen species; oxidative stress; hypoxia


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