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 coli was the predominant pathogen together with Streptococcus faecalis, Pseudomonas, and Lactobacillus species. 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. Copyright 1998 Academic Press.
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 coli was the predominant pathogen together with Streptococcus faecalis, Pseudomonas, and Lactobacillus species. 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. Copyright 1998 Academic Press.
Authors: Misha D P Luyer; Jan A Jacobs; Anita C E Vreugdenhil; M'hamed Hadfoune; Cornelis H C Dejong; Wim A Buurman; Jan Willem M Greve Journal: Ann Surg Date: 2004-02 Impact factor: 12.969