The objective of this study is to determine if heat stress prior to endotoxemia diminishes cardiopulmonary dysfunction by attenuating the cytokine inflammatory response. Rats were assigned to either: 1) neutropenia; 2) heat; 3) neutropenia, LPS; or 4) heat, neutropenia, LPS. Heart rate, blood gases, and blood, lung lavage, and lung mRNA for tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and macrophage inflammatory protein (MIP)-2 were measured. Heat given before LPS resulted in a similar A-a O2 gradient as the heat-alone and neutropenic groups (8 ± 8 versus 8 ± 7 versus 4 ± 3 mm Hg) and a lower A-a O2 gradient when compared to the neutropenic, LPS rats (8 ± 8 versus 22 ± 8 mm Hg, p < 0.003). Blood, lung lavage, and lung mRNA for TNF-α, IL-1β, and MIP-2 were similar in the LPS rats regardless of heat. Heart rate was similar in both LPS groups but higher than non-LPS groups. Heat pretreatment attenuates lung injury in the neutropenic, endotoxemic rat but not by decreasing TNF-α, IL-1β, or MIP-2 in the lung. Heat prior to LPS did not prevent cardiac dysfunction in neutropenic rats.
- Acute lung injury
- Macrophage inflammatory protein-2
- Tumor necrosis factor-α