Pulmonary Protection in Heat Stressed Rats is Associated with Macrophage Inflammatory Protein-2 (MIP-2) Production by Alveolar Macrophages • 201

Abstract

We investigated whether heat stress protects the lung and cardiovascular system from injury by modifying cytokine production. Methods: 16 rats were randomly assigned to the normothermia group(NG) (n=8) or heat stress group (HSG)(n=8). The HSG maintained a temperature of 42°C for 10 min by external heat. 20 hrs later, the rats were ventilated and given 0.5 mg/kg E. Coli LPS. Blood was collected for blood gases, TNF, IL-10 and MIP-2 at 0, 2, 4, 5 hrs. At 5 hrs, alveolar macrophages (AM) were obtained and incubated for 24 hrs and production of heat shock protein (HSP)was determined. Results: Only the AM of HSG rats produced HSP. By 5 hrs, HSG had a lower A-a O2 gradient compared to the NG rats (209±13 vs 294±22 mm Hg, p<0.01). AM from the HSG produced more MIP-2 (1723±288 vs 751±264 pg/ml, p<0.01). The A-a O2 gradient inversely correlated with MIP-2 in the AM supernatant (r=-0.65, p<0.01, Fig). Hypotension was less in the HSG between 0.5 and 2 hrs but not subsequently. Serum MIP-2 was elevated in the HSG compared to NGat 2 hrs (89.8±32.8 vs 26.5±4.0ng/ml, p<0.02). Detection of TNF, IL-10, and NO in the blood and AM supernatant was similar in both groups. Conclusions: Heat stress-induced lung protection in acute endotoxemia is associated with MIP-2 production by alveolar macrophages. Mechanism of protection from endotoxemia via MIP-2 in heat stressed rats needs to be explored.