• Sabrina M Heidemann and Maria Glibetic.
• Departments of Pediatric Critical Care Medicine and Clinical Pharmacology, Children's Hospital of Michigan, Wayne State University, 3901 Beaubien Blvd., Detroit, Michigan, 48201-2196, USA. sheidema@med.wayne.edu
• Inflammation. 2005 Feb 1; 29 (1): 47-53.

AbstractThe 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.

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