Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Clinical Trial
Short-term effects of phenylephrine on systemic and regional hemodynamics in patients with septic shock: a crossover pilot study.
Clinical studies evaluating the use of phenylephrine in septic shock are lacking. The present study was designed as a prospective, crossover pilot study to compare the effects of norepinephrine (NE) and phenylephrine on systemic and regional hemodynamics in patients with catecholamine-dependent septic shock. In 15 septic shock patients, NE (0.82 +/- 0.689 microg x kg(-1) x min(-1)) was replaced with phenylephrine (4.39 +/- 5.23 microg x kg(-1) x min(-1)) titrated to maintain MAP between 65 and 75 mmHg. ⋯ In addition, phenylephrine increased arterial lactate concentrations as compared with NE infusion (1.7 +/- 1.0 vs. 1.4 +/- 1.1 mM; P < 0.05). After switching back to NE, all variables returned to values obtained before phenylephrine infusion except creatinine clearance and gastric tonometry values. Our results suggest that for the same MAP, phenylephrine causes a more pronounced hepatosplanchnic vasoconstriction as compared with NE.
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Increased intestinal/epithelial permeability in sepsis and endotoxemia has been noted to be induced by proinflammatory cytokines such as interferon-gamma, TNF-alpha, and IL-1beta. The p38 mitogen-activated protein kinase (MAPK) signaling pathway plays an important role in regulating the inflammatory response induced by these cytokines. We tested the hypothesis that epithelial permeability changes are regulated through the p38 MAPK signaling pathway. ⋯ Treatment with SB203580 completely blocked p38 activity with transient inhibition of p38 phosphorylation. SB203580 also prevented the CytoMix-induced permeability increase and reduced NO, IL-6, and IL-8 levels. The results suggest that p38 MAPK plays an important role in regulating epithelial barrier function during inflammation.
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Recent clinical studies have shown a sex dimorphism of morbidity and mortality due to shock, trauma, and sepsis, with females tolerating these insults better than males. Experimental animal studies have suggested that sex hormones have a pivotal role in this dimorphism. In the present investigation, a prospective cohort study at a university level-1 trauma center was conducted to evaluate the association between sex hormones and alterations in coagulation and inflammation. ⋯ In men, the E2-Pr was also negatively correlated with the time to onset of clot formation (P = 0.03). Sex hormone levels (or their ratios) were not correlated to platelet count or international normalized ratios. These findings provide evidence that sex hormone levels in the early posttraumatic period are significantly associated with alterations in the hemostatic and inflammatory response to trauma.
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The prognostic value of procalcitonin (PCT) in patients with sepsis at the emergency department (ED) has not been evaluated. We conducted a prospective observational study to compare the prognostic value of PCT on sepsis and compared with a validated score, Mortality in Emergency Department Sepsis (MEDS) score, and C-reactive protein (CRP) in the setting of ED of an urban, university-based medical center. Five hundred twenty-five consecutive adult patients admitted to the ED fulfilling the American College of Clinical Pharmacists/Society of Critical Care Medicine Consensus Conference definition of sepsis were prospectively enrolled. ⋯ Overall, MEDS score has the best discriminative capability among the three tested markers. Under the best cutoff value, PCT was the most sensitive, and MEDS score was the most specific marker. We suggest further combining the information on PCT and MEDS score to enhance the accuracy in predicting ED sepsis mortality.