Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2025
The effects of dexmedetomidine on liver injury in rats with experimental sepsis: A histopathological and immunohistochemical study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Keleş Ömer Faruk, Sayhan Kaplan Havva, Çiçek Hacı Ahmet, Palabiyik Onur, Yener Zabit
Аннотация
BACKGROUND: In the rat sepsis model, the protective effect of dexmedetomidine (Dex) in sepsis-induced tissue injuries by reducing inflammation is still unclear, and research is ongoing to determine whether Dex modulates sepsis-induced tissue injury. To investigate the effect of Dex on liver injury in sepsis rats histopathologically and immunohistochemically.
METHODS: In this study, sepsis was induced in rats by 10 ml/kg E. coli injection and the protective efficacy of Dex against liver damage was investigated with histopathological and immunohistochemical findings by intraperitoneal administration of 100 mcg/kg Dex.
RESULTS: In our results, the most striking and basic morphological changes in the liver tissues of sepsis group rats were neutrophil leukocyte infiltrations in and around the vessels. In Dex-treated groups, neutrophil leucocyte infiltrations were more prominent and marked dilatations were observed in the vessels. The fact that inflammatory reactions were more prominent in the Dex-treated groups was thought to be related to the increase in vascular permeability due to Dex's vasodilation effect.
CONCLUSION: according to the histopathological and immunohistochemical findings obtained in the present study, we conclude that Dex did not alleviate sepsis-induced liver inflammation in a rat sepsis model.
METHODS: In this study, sepsis was induced in rats by 10 ml/kg E. coli injection and the protective efficacy of Dex against liver damage was investigated with histopathological and immunohistochemical findings by intraperitoneal administration of 100 mcg/kg Dex.
RESULTS: In our results, the most striking and basic morphological changes in the liver tissues of sepsis group rats were neutrophil leukocyte infiltrations in and around the vessels. In Dex-treated groups, neutrophil leucocyte infiltrations were more prominent and marked dilatations were observed in the vessels. The fact that inflammatory reactions were more prominent in the Dex-treated groups was thought to be related to the increase in vascular permeability due to Dex's vasodilation effect.
CONCLUSION: according to the histopathological and immunohistochemical findings obtained in the present study, we conclude that Dex did not alleviate sepsis-induced liver inflammation in a rat sepsis model.