The effect of heat on cytokine production in rat endotoxemia.
Crit Care Med
; 28(5): 1465-8, 2000 May.
Article
en En
| MEDLINE
| ID: mdl-10834697
ABSTRACT
OBJECTIVE:
To determine whether heat stress protects the endotoxemic rat by up-regulation of the counterinflammatory cytokine interleukin (IL)-10, thereby 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 temperature of >42 degrees C (107.6 degrees F) rectally for 10-15 mins; 20 hrs later, all rats were intubated, paralyzed, and ventilated. After jugular venous and arterial catheterization, endotoxin was given intravenously. Arterial blood was removed at 0, 2, 4, and 5 hrs for blood gases, tumor necrosis factor (TNF)-alpha, nitric oxide metabolites (NO), IL-10, and macrophage inflammatory protein (MIP)-2. The alveolar macrophages were removed, counted, and then incubated for 24 hrs. The supernatant was analyzed for TNF-alpha, 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 MAINRESULTS:
Alveolar-arterial oxygen gradient was lower in the heat stress group at 4 and 5 hrs after endotoxemia. Plasma and alveolar macrophage supernatant concentrations of TNF-alpha, NO, and IL-10 were not affected by heat. Plasma and alveolar macrophage supernatant MIP-2 concentrations were higher in endotoxemic rats receiving heat pretreatment compared 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 and alveolar macrophage production of MIP-2 in endotoxemia. The mechanism of heat-conferred pulmonary protection in endotoxemia remains unclear. Alveolar macrophages do not produce IL-10 in endotoxemia. The increased MIP-2 production by heated alveolar macrophages was not attributable to alterations in production of either TNF-alpha or IL-10. The significance of increased MIP-2 by endotoxin-exposed alveolar macrophages in heated rats is unknown.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Citocinas
/
Macrófagos Alveolares
/
Trastornos de Estrés por Calor
/
Endotoxemia
/
Fiebre
Límite:
Animals
Idioma:
En
Revista:
Crit Care Med
Año:
2000
Tipo del documento:
Article
País de afiliación:
Estados Unidos