Abstract

Background.Bacterial translocation is thought to be responsible for infectious complications after hemorrhagic shock. The aim of this study is to investigate the effects of granulocyte colony-stimulating factor (G-CSF) treatment on bacterial translocation in starved or fed animals subjected to hemorrhagic shock.Materials and Methods.Fifty Wistar albino rats (200–275 g) were divided into six groups such as naive control (n= 7), G-CSF treatment (n= 7), hemorrhagic shock in starved rats (n= 9), hemorrhagic shock in fed rats (n= 9), G-CSF treatment 24 h before hemorrhagic shock in starved rats (n= 9), and G-CSF treatment 20 min after hemorrhagic shock in fed rats (n= 9). Hemorrhagic shock was induced by withdrawal of 2.1 ml/100 g blood via a carotid arterial cannulae placed under sodium pentobarbital anesthesia. Twenty-four hours later, mesenteric lymph nodes, liver, spleen, and peripheral blood samples were evaluated by using a quantitative microbiological technique and the numbers of colony-forming units were compared between groups.Results.No bacteria was detected in samples from naive controls or G-CSF-treated unshocked rats. In animals subjected to hemorrhage,Escherichia coliwas the predominant pathogen together withStreptococcus faecalis, Pseudomonas,andLactobacillusspecies. In this model, starvation augmented the magnitude of bacterial translocation while G-CSF treatment has virtually abolished it.Conclusion.Under experimental conditions, preshock starvation increases gut-derived bacterial translocation and administration of G-CSF before or after hemorrhagic insult significantly reduces it.

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