Development of a model for anemia of inflammation that is relevant to critical care
Autor: | Marcus J. Schultz, Sebastian A. J. Zaat, Ana Motos, Gianluigi Li Bassi, Antoni Torres, Nicole P. Juffermans, Paolo Pelosi, Margit Boshuizen, Tarek Senussi, Eli Aguilera, Francesco Idone, Robin van Bruggen |
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Přispěvatelé: | Graduate School, ACS - Heart failure & arrhythmias, AII - Inflammatory diseases, Landsteiner Laboratory, Medical Microbiology and Infection Prevention, AII - Infectious diseases, Intensive Care Medicine, ACS - Pulmonary hypertension & thrombosis, ACS - Diabetes & metabolism, ACS - Microcirculation |
Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
Mean arterial pressure
Resuscitation Anemia Iron Physiology Anèmia Critical Care and Intensive Care Medicine Infections Sepsis 03 medical and health sciences 0302 clinical medicine Hepcidin Medicine Animal model Unitats de cures intensives chemistry.chemical_classification Intensive care units biology business.industry Research lcsh:Medical emergencies. Critical care. Intensive care. First aid 030208 emergency & critical care medicine lcsh:RC86-88.9 medicine.disease Infeccions 030228 respiratory system chemistry Transferrin Anemia of inflammation ICU Infection Toxicity biology.protein Base excess business Ferro |
Zdroj: | Intensive Care Medicine Experimental Intensive Care Medicine Experimental, 7(Suppl 1):47. Springer Science + Business Media Dipòsit Digital de la UB Universidad de Barcelona Intensive Care Medicine Experimental, Vol 7, Iss S1, Pp 1-11 (2019) |
ISSN: | 2197-425X |
Popis: | Background Anemia of inflammation (AI) is common in critically ill patients. Although this syndrome negatively impacts the outcome of critical illness, understanding of its pathophysiology is limited. Also, new therapies that increase iron availability for erythropoiesis during AI are upcoming. A model of AI induced by bacterial infections that are relevant for the critically ill is currently not available. This paper describes the development of an animal model for AI that is relevant for critical care research. Results In experiments with rats, the rats were inoculated either repeatedly or with a slow release of Streptococcus pneumoniae or Pseudomonas aeruginosa. Rats became ill, but their hemoglobin levels remained stable. The use of a higher dose of bacteria resulted in a lethal model. Then, we turned to a model with longer disease duration, using pigs that were supported by mechanical ventilation after inoculation with P. aeruginosa. The pigs became septic 12 to 24 h after inoculation, with a statistically significant decrease in mean arterial pressure and base excess, while heart rate tended to increase. Pigs needed resuscitation and vasopressor therapy to maintain a mean arterial pressure > 60 mmHg. After 72 h, the pigs developed anemia (baseline 9.9 g/dl vs. 72 h, 7.6 g/dl, p = 0.01), characterized by statistically significant decreased iron levels, decreased transferrin saturation, and increased ferritin. Hepcidin levels tended to increase and transferrin levels tended to decrease. Conclusions Using pathogens commonly involved in pulmonary sepsis, AI could not be induced in rats. Conversely, in pigs, P. aeruginosa induced pulmonary sepsis with concomitant AI. This AI model can be applied to study the pathophysiology of AI in the critically ill and to investigate the effectivity and toxicity of new therapies that aim to increase iron availability. Electronic supplementary material The online version of this article (10.1186/s40635-019-0261-2) contains supplementary material, which is available to authorized users. |
Databáze: | OpenAIRE |
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