latrodMCtm: Heat stress prior to sepsis has been shown to cardiopulroonary dysfunction and improve survival. The objective of this study was to determine if heat stress protects the lung and cardiovascular system from injury by modifying the cytokinc response. Methods: 16 rats were assigned to the normothennia group (n=8) or heat stress group (n=8). The heat stress group maintained a temperature of 42°C for 10 min by external heat. 20 hrs later, the rats were ventilated, catheterized and given 0.5 mg/lcg E. Colt LPS by IV infusion. Arterial blood was obtained for blood gases. TNF. interleukin (ID-10, and macroohaee inflammatory nrotein (MEPV2 at 0. 2. 4. 5 hrs. At 5 hrs, alveolar macrophages (AM) were obtained and incubated for 24 hrs. Heat shock protein was determined by Western Mot on the AM and spieaocytes. Result: Heat shock protein was present in the AM and spleaocytes of ' only the heated rats. By 5 hrs, heat stressed rats had a lower A-a gradient than non-heat stressed rats (209+13 vs 294+22 mm Hg. p<0.01). AM from heat stressed rats produced more Mff-2 than noo-beated rats (1723+288 vx 751+264 pg/ml, p<0.01). The A-a gradient inversely correlated with MIP-2 concentration in the AM supernatant (r=-0.65, pO.Ol, fig). Hypotension was less in the hat stressed rats between 0.5 and 2 hrs, but not subsequently. Serum MIP-2 was elevated in the heat stressed rats at 2 hrs (89.8+32.8 vs 26.5+4.0ng/ml, p<0.02) when compared to Don-heated rats. Serum TNF, EL-10, and NO concentrations were similar in both groups. There was no significant difference in the production of TNF and NO by AM in heat and non-heat stressed rats. AM did not produce 1L-10 in either group. CoachifMMs: Heat stress induced pulmonary protection in acute endotoxemia appears to be secondary to MIP-2 production. Alveolar macrophages play an important role in acute lung injury by signaling PMN chemotaxis. Mechanism of protection from endotoxemia via MIP-2 in beat stressed rats needs to be explored.