Abstract
Objective: to analyze variations in body temperature and in plasma nitrate and lactate concentrations in rats submitted to the experimental sepsis model.Method: a total of 40 rats divided equally into five groups. The induction of endotoxemia was performed with intravenous administration of lipopolysaccharide, 0.5 mg/Kg, 1.5 mg/Kg, 3.0 mg/Kg, and 10 mg/Kg, respectively. The control group received 0.5 mL of saline solution. The experiment lasted six hours, with evaluations performed at 0 (baseline data), 2nd, 4th, and 6thhours.Results: The animals that received doses up to 3.0 mg/kg showed a significant increase in body temperature compared to the group with 10 mg/kg, which showed a decrease in these values. The increase in plasma nitrate and lactate concentrations in the groups with lipopolysaccharide was significantly higher than in the group that received the saline solution and was correlated with the increase in body temperature.Conclusion: the variations in body temperature observed in this study showed the dose-dependent effect of lipopolysaccharide and were correlated with the increase in the concentrations of nitrate and plasma lactate biomarkers. The implications of this study are the importance of monitoring body temperature, together with the assessment of these pathophysiological markers, which suggest worsening in the prognosis of sepsis.
Highlights
Despite the large number of studies available in the literature, limitations are still found in the understanding of the pathophysiological mechanisms, which result in high rates of sepsis-related morbidity and mortality in Intensive Care Units (ICUs)(1)
The clinical course of the disease can lead to a worsening of the prognosis, when changes occur to the stages of severe sepsis and septic shock[2]
This study shows, for the first time, the correlation between body temperature and mediators that participate in the pathophysiology of sepsis and septic shock in animals submitted to experimental sepsis with different doses of LPS
Summary
Despite the large number of studies available in the literature, limitations are still found in the understanding of the pathophysiological mechanisms, which result in high rates of sepsis-related morbidity and mortality in Intensive Care Units (ICUs)(1). The clinical course of the disease can lead to a worsening of the prognosis, when changes occur to the stages of severe sepsis and septic shock[2]. This change represents a mortality rate ranging from 10% to 40%(3-4). The mechanisms that result in an ineffective thermo-regulation during the most severe stages of sepsis, mainly related to hypothermia, remain misunderstood[1,5]. The exacerbated inflammatory response and infection are determining factors in the clinical evolution of sepsis[6], which accompanies the increase in the production of pro-inflammatory cytokines (interleukin – (IL-) 1β, tumor necrosis factor – (TNF-) α, and interferon – (IFN-) γ) or of antiinflammatory cytokines (interleukin – (IL-) 10, and transforming growth factor – (TGF-) β)(7-8). An increase in the production of reactive oxygen species is observed, for example, Nitric Oxide (NO)(9)
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