| Autor: |
Hofstetter, C., Boost, K. A., Flondor, M., Basagan-Mogol, E., Betz, C., Homann, M., Muhl, H., Pfeilschifter, J., Zwissler, B. |
| Předmět: |
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| Zdroj: |
Acta Anaesthesiologica Scandinavica; Aug2007, Vol. 51 Issue 7, p893-899, 7p, 4 Charts, 1 Graph |
| Abstrakt: |
Background: Volatile anesthetics and hypothermia attenuate the inflammatory response. We aimed to compare the anti-inflammatory effects of sevoflurane and mild hypothermia during experimental endotoxemia in the rat. Methods: Anesthetized, ventilated Sprague–Dawley (SD) rats were randomly treated as follows ( n = 6 per group): lipopolysaccharide (LPS) only, animals received LPS [LPS 5 mg/kg, intravenously (i.v.)] with no further treatment. In the LPS-hypothermia group, rats were cooled down to a temperature of 33 °C 15 min after LPS-injection (LPS 5 mg/kg i.v.). In animals of the LPS-sevoflurane group, sevoflurane inhalation (1 MAC) was initiated 15 min after induction of endotoxemia. The LPS-sevoflurane-hypothermia group received combined sevoflurane and hypothermia 15 min after induction of endotoxemia. A Sham group served as control without endotoxemia or treatment. After 4 h of endotoxemia, plasma levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-10 were measured. Alveolar macrophages (AM) were ex vivo cultured for nitrite assay. Results: Inhalation of sevoflurane significantly attenuated plasma levels of TNF-α (–60%, P < 0.05) and IL-1β (–68%, P < 0.05) as compared with the LPS-only group. Hypothermia and its combination with sevoflurane significantly reduced TNF-α levels (–46% and –58%, each P < 0.05), but not IL-1β. Application of mild hypothermia and also its combination with sevoflurane resulted in a significant increase in plasma IL-10 as compared with endotoxemic controls. Nitrite release from AM was found to be significantly suppressed by sevoflurane (–83%), hypothermia (–73%) and by the combination of both (–67%) ( P < 0.05, each). Conclusion: Our data suggest that sevoflurane and mild hypothermia attenuate the inflammatory response during endotoxemia in vivo thus contributing to their beneficial role in clinical organ protection. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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