Hernández-Jiménez C, Olmos-Zúñiga JR, Jasso-Victoria R, Gaxiola-Gaxiola M, Baltazares-Lipp M, Sánchez-Arrozena LS, Gutiérrez-González LH

Language: Spanish
References: 48
Page: 452-460
PDF size: 439.84 Kb.

ABSTRACT

Introduction. Acute lung injury (ALI) is a pathological condition characterized by injury in the alveolar-capillary membrane that triggers local and systemic inflammation. Endothelin (ET) is a protein that regulates immune response and constricts blood vessels; when it is over-expressed, it may contribute to high blood pressure and lung injury. This work tries to determine if propofol may decrease hemodynamic, gasometric, microscopic, ET-1 plasmatic concentration, and immuno-histochemical alterations in an experimental model of oleic acid-induced acute lung injury. Materials and methods. Animals were classified into three groups (n = 6): group I was the control group; in group II, there was oleic acid-induced ALI with no treatment, and group III with propofol pre-treatment and oleic acid-induced ALI. Results. All animals survived until the end of the study, and 100% of group II and group III developed ALI, with hemodynamic, gasometric and gravimetric alterations. However, group III showed less inflammatory infiltration and lower ET-1 expression in lung tissue. Conclusions. Pretreatment with propofol in a canine model of OA-induced ALI indicates that the drug has anti-inflammatory action, with a potential therapeutic role against progression of anti-inflammation and lung damage.

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