Heat stress protects the cardiopulmonary system by increasing monocyte chemoattractant protein-1 production in rat endotoxemia

Amit P. Sarnaik, Sabrina M. Heidemann, Ashok P. Sarnaik

Research output: Contribution to journalArticlepeer-review

Abstract

Introduction: Heat stress prior to sepsis has been shown to attenuate cardiopulmonary dysfunction and improve survival. Monocyte chemoattractant protein-1 (MCP-1) may be protective in endotoxemia by stimulating the anti-inflammatory response. The objective of this study was to determine if heat stress decreases injury in endotoxemia by increasing the production of MCP-1. Methods: 16 rats were assigned to normothermia (n=8) or the heat stress group (n=8). The heat stress group was maintained at a temperature of 42°C for 10 min by external heat. 20 hrs later, the rats were ventilated, catheterized and given 0.5 mg /kg E.coli LPS by IV infusion. Arterial blood was obtained for blood gases, tumor necrosis factor (TNF)-α, interleukin (IL)-10, nitric oxide (NO), and MCP-1 at 0,2,4,5 hrs. Alveolar macrophages were obtained at 5 hrs and incubated in media for 24 hrs. The supernatant was analyzed for MCP-1, IL-10, NO, and TNF-α. Results: The serum MCP-1 levels were significantly higher in the heated group compared to the normothermia group at 2 hrs (p<0.03, figure). Heat stressed rats had a higher blood pressure at 60 minutes (108 ± 7 vs 77 ± 6 mm Hg, p<0.0005), and a lower A-a O2 gradient at 5 hrs (205 ± 16 vs 294 ± 22 torr, p<0.01) compared to normothermic rats. Alveolar macrophages did not produce any MCP-1 or IL-10. Serum TNF, IL-10, and NO concentration were similar in both groups. Conclusions: Cardiopulmonary protection by heat stress in acute endotoxemia could be secondary to stimulation of MCP-1 production. MCP-1 may act to increase the counter-inflammatory response, however the mechanism of action of MCP-1 is unclear and requires further investigation.

Original languageEnglish
Pages (from-to)A57
JournalCritical Care Medicine
Volume27
Issue number1 SUPPL.
DOIs
StatePublished - 1999

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