Heat stress protects against lung injury in the neutropenic, endotoxemic rat.

Abstract

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)-alpha, interleukin (IL)-1beta, and macrophage inflammatory protein (MIP)-2 were measured. Heat given before LPS resulted in a similar A-a O(2) gradient as the heat-alone and neutropenic groups (8 +/- 8 versus 8 +/- 7 versus 4 +/- 3 mm Hg) and a lower A-a O(2) 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-alpha, IL-1beta, 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-alpha, IL-1beta, or MIP-2 in the lung. Heat prior to LPS did not prevent cardiac dysfunction in neutropenic rats.