Judit Tóth1, Ildikó Beke Debreceni1, Mariann Berhés2, Endre Hajdú2, Ádám Deák3, Katalin Pető3, Judit Szabó4, Norbert Németh3, Béla Fülesdi2, János Kappelmayer1. 1. Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. 2. Department of Anesthesiology and Intensive Therapy, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. 3. Department of Operative Techniques and Surgical Research, Institute of Surgery, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. 4. Department of Medical Microbiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Abstract
OBJECTIVE: In a fulminant porcine sepsis model, we determined the kinetics of hypoxia induced changes in relation to sepsis parameters and markers of organ damage. METHODS: Female pigs were challenged by live Escherichia coli and samples were analysed up to 4 hours. Bone marrow reactions were determined by analysing immature forms of peripheral blood cells by a hematology analyser and light microscopy. Platelet mitochondrial membrane depolarisation was determined by flow cytometry. RESULTS: Core temperature, modified shock index and lactate levels all became significantly elevated compared to baseline values at 4 hours in septic animals. At 2 hours already the reticulocyte count, nucleated red blood cell count and the absolute number of dysplastic platelets became significantly elevated. The platelet mitochondrial membrane depolarisation was significantly decreased by 2 hours in septic animals compared to the baseline values and to control animals. No massive organ damage was evident during the 4-hour observation period, but uric acid levels in septic animals became significantly elevated already by 2 hours. CONCLUSIONS: In this Escherichia coli induced porcine model, severe sepsis was evident by conventional criteria at 4 hours while several - mostly hypoxemia induced - biomarkers were already altered by 2 hours.
OBJECTIVE: In a fulminant porcine sepsis model, we determined the kinetics of hypoxia induced changes in relation to sepsis parameters and markers of organ damage. METHODS: Female pigs were challenged by live Escherichia coli and samples were analysed up to 4 hours. Bone marrow reactions were determined by analysing immature forms of peripheral blood cells by a hematology analyser and light microscopy. Platelet mitochondrial membrane depolarisation was determined by flow cytometry. RESULTS: Core temperature, modified shock index and lactate levels all became significantly elevated compared to baseline values at 4 hours in septic animals. At 2 hours already the reticulocyte count, nucleated red blood cell count and the absolute number of dysplastic platelets became significantly elevated. The platelet mitochondrial membrane depolarisation was significantly decreased by 2 hours in septic animals compared to the baseline values and to control animals. No massive organ damage was evident during the 4-hour observation period, but uric acid levels in septic animals became significantly elevated already by 2 hours. CONCLUSIONS: In this Escherichia coli induced porcine model, severe sepsis was evident by conventional criteria at 4 hours while several - mostly hypoxemia induced - biomarkers were already altered by 2 hours.
Entities:
Keywords:
Immature red blood cells and platelets; platelet apoptosis; sepsis