The effect of heat on cytokine production in rat endotoxemia

Citation
Sm. Heidemann et al., The effect of heat on cytokine production in rat endotoxemia, CRIT CARE M, 28(5), 2000, pp. 1465-1468
Citations number
31
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
28
Issue
5
Year of publication
2000
Pages
1465 - 1468
Database
ISI
SICI code
0090-3493(200005)28:5<1465:TEOHOC>2.0.ZU;2-B
Abstract
Objective: To determine whether heat stress protects the endotoxemic rat by up-regulation of the counterinflammatory cytokine interleukin (IL)-10, the reby attenuating the inflammatory response. Design: A total of 16 rats were assigned to either the heat stress group (n = 8) or the control group (n = 8). The heat stress group was warmed to a t emperature of >42 degrees C (107.6 degrees F) rectally for 10-15 mins; 20 h rs later, all rats were intubated, paralyzed, and ventilated. After jugular venous and arterial catheterization, endotoxin was given intravenously. Ar terial blood was removed at 0, 2, 4, and 5 hrs for blood gases, tumor necro sis factor (TNF)-alpha, nitric oxide metabolites (NO), IL-10, and macrophag e inflammatory protein (MIP)-2, The alveolar macrophages were removed, coun ted, and then incubated for 24 hrs. The supernatant was analyzed for TNF-al pha, NO, IL-10, and MIP-2. Setting: University research laboratory, Subjects: Male Sprague-Dawley rats (n = 16). Interventions: Administration of heat before endotoxin infusion. Measurements and Main Results: Alveolar-arterial oxygen gradient was lower in the heat stress group at 4 and 5 hrs after endotoxemia. Plasma and alveo lar macrophage supernatant concentrations of TNF-alpha, NO, and IL-10 were not affected by heat. Plasma and alveolar macrophage supernatant MIP-2 conc entrations were higher in endotoxemic rats receiving heat pretreatment comp ared with controls. Conclusions: Our study demonstrates that heat leads to pulmonary protection of short duration in severe endotoxemia. This protection was not mediated by plasma TNF-alpha, IL-10, or NO. Contrary to our hypothesis, pretreatment with heat increased rather than decreased the plasma MIP-2 concentration a nd alveolar macrophage production of MIP-2 in endotoxemia. The mechanism of heat-conferred pulmonary protection in endotoxemia remains unclear. Alveol ar macrophages do not produce IL-10 in endotoxemia. The increased MIP-2 pro duction by heated alveolar macrophages was not attributable to alterations in production of either TNF-alpha or IL-10. The significance of increased M IP-2 by endotoxin-exposed alveolar macrophages in heated rats is unknown.