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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The optimal type and amount of fluid for resuscitation of injured patients in hemorrhagic hypovolemic shock remains controversial. Use of deferoxamine, an iron chelator and oxygen-free radical scavenger, and hespan (hydroxyethyl starch), a colloid plasma expander, was evaluated in a rat hemorrhagic shock model. Eighty Sprague-Dawley male rats were utilized in four experiments. ⋯ In experiment 4 (n = 12), a combination of deferoxamine (100 mg/kg) and Hespan (3.75 and 7.5 mL) was used. Deferoxamine (100 mg/kg) complexed with 7.5 mL of Hespan was found the most beneficial resuscitation. This conjugate could be a choice as a resuscitative adjuvant in hypovolemic shock without any side effects.
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This study was conducted to investigate the extent of platelet-leukocyte adhesion and platelet, monocyte, and neutrophil activation in septic patients and to analyze whether these variables correlate with the severity of sepsis. Forty-seven patients consecutively admitted to the operative ICU of a University Medical Centre and 12 control patients prior to elective surgery were included in this prospective cohort study. Patients were evaluated daily for sepsis criteria and sepsis-associated organ failure assessment (SOFA) score was used to describe the extent of sepsis-associated organ failure. ⋯ Higher values for platelet-neutrophil adhesion were observed in patients with uncomplicated sepsis compared either with controls or to patients with septic shock. An inverse relation between severity of sepsis and extent of platelet-neutrophil adhesion was also obvious from correlation analysis. The results indicate that flow cytometry can be used to measure these parameters of cell activation in sepsis and that activation of platelets and monocytes as well as adhesion of platelets to neutrophils does play a role in the development of organ dysfunction.
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Systemic inflammation triggered by insults like sepsis and acute pancreatitis may play a role in development of indirect acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Because little is known about the course of systemic inflammation on the days preceding diagnosis of ARDS, we prospectively monitored immune inflammatory status in 52 patients at risk and we assessed the presence of ALI and ARDS on day 7 after admission to the intensive care unit. On admission, serum interleukin (IL) 8, IL-6, and soluble IL-2 receptor concentrations were significantly higher in patients with subsequent ALI (n = 18) than in patients without ALI (n = 30). ⋯ Among 11 patients with acute pancreatitis, ALI patients had significantly higher IL-8, IL-6, and phagocyte CD11b expression levels than did non-ALI patients, whereas among 14 patients with massive transfusion, respective findings in ALI and non-ALI patients were comparable. Results give credence to the view that systemic inflammation plays a role in development of ALI triggered by pancreatitis, but not in that by massive transfusion. This finding, if confirmed in studies with sufficient statistical power, suggests that the patients with massive transfusion do not necessarily benefit from novel biotherapies aimed at altering the course of systemic inflammation.
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Despite the established success of surfactant application in neonates, the use of surfactant in older children is still a matter of discussion. We hypothesized that surfactant application in children with acute respiratory distress syndrome (ARDS) secondary to a pulmonary or systemic disease or after cardiac surgery improves pulmonary function. We also asked whether repeated treatment could further improve pulmonary function. ⋯ We conclude that a single surfactant application improves pulmonary function in children with ARDS. A second application of surfactant showed no further benefit. Outcome was not affected in our study population.
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Hyperoxia and tumor necrosis factor-alpha (TNFalpha) are two canonical signals centrally involved in the pathophysiology of acute lung injury. We have attempted to elucidate the effects of these two stimuli on the signal transduction pathways of lung parenchymal cells. In cultured human lung epithelial cells, exposure to hyperoxia alone (95% oxygen) did not affect NF-kappaB activation or degradation of the NF-kappaB inhibitory protein, IkappaB alpha. ⋯ Hyperoxia alone did not activate the intercellular adhesion molecule-1 (ICAM-1) promoter, but augmented TNFalpha-mediated activation of the ICAM-1 promoter. These data demonstrate that while hyperoxia alone does not affect activation of NF-kappaB, hyperoxia prolongs TNFalpha-mediated activation of NF-kappaB. The mechanism of this effect involves, in part, prolonged degradation of IkappaB alpha resulting from prolonged activation of IKK.