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      Effects of a New Extracorporeal System Using CTR on Mortality and Inflammatory Responses to Bacterial Toxin-Induced Multiple Organ Dysfunction Syndrome in Rabbits

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          Background/Aims: In the pathogenesis of multiple organ dysfunction syndrome (MODS) caused by bacterial infection, a complex series of systemically secreted bacterial toxins and cytokines are intensely associated. Our previous study demonstrated that a new adsorbent, CTR, was capable of removing cytokines and toxic shock syndrome toxin-1 (TSST-1) in vitro. Moreover, extracorporeal treatment with CTR reduced the high mortality rate and inhibited inflammatory responses in endotoxin-induced shock in rats. However, it is unclear whether CTR treatment will be an effective therapy for MODS. Here, we demonstrated the efficacy of a new extracorporeal system using CTR on MODS induced by bacterial toxins in rabbits. Methods: Direct hemoperfusion (DHP) apheresis with or without CTR for 120 min was performed in rabbits that had been intravenously infused with endotoxin and TSST-1. The mean arterial pressure was recorded and the plasma toxin and cytokine concentrations were measured during the treatment period. Mortality was assessed up to 7 days after exposure to the toxins. In addition, tissues specimens were examined using microscopy. Results: The mortality rates at 7 days after the injection of the toxins were 90 and 10% for the control and CTR groups, respectively. The plasma concentrations of TSST-1, tumor necrosis factor and interleukin-1 beta in the CTR group were significantly lower than those in the control group. Histopathological examination revealed that tissue damage, such as necrosis and depletion of lymphocytes in the spleen and mesenteric lymph node, was reduced in the CTR group, compared with that in the control group, at 24 h after toxin infusion. Conclusion: The new adsorbent CTR improved the mortality rate in a MODS rabbit model by adsorbing TSST-1 and cytokines. Further development of CTR may expand the scope of extracorporeal therapies for patients with MODS.

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          Most cited references 10

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          American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference

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            Nosocomial infections in pediatric patients: a European, multicenter prospective study. European Study Group.

            To determine the site and bacterial epidemiology of nosocomial infections (NIs) in children. 6-month prospective study with periodic chart review during hospitalization using a uniform prospective questionnaire in each unit, analyzed at a coordinating center. 20 units in eight European countries: 5 pediatric intensive care units (PICUs), 7 neonatal units, 2 hematology-oncology units, 8 general pediatric units. All children hospitalized during the study period with an NI according to Centers for Disease Control and Prevention criteria. The overall incidence of NI was 2.5%, ranging from 1% in general pediatric units to 23.6% in PICUs. Bacteria were responsible for 68% (gram-negative bacilli, 37%; gram-positive cocci, 31%), Candida for 9%, and viruses for 22% of cases. The proportion of lower respiratory tract infections was 13% in general pediatric units and 53% in PICUs. Bloodstream infections were most frequent in neonatal units (71% of NIs) and were associated with a central venous catheter in 66% of cases. Coagulase-negative Staphylococcus (CNS) was the main pathogen. Eleven percent of NI were urinary tract infections. Gastrointestinal infections were most commonly viral and accounted for 76% of NIs in general pediatric units. The prevalence of antimicrobial resistance depended on the type of unit. The highest rates were observed in PICUs: 26.3% of Staphylococcus aureus and 89% of CNS were methicillin-resistant, and 37.5% of Klebsiella pneumoniae had an extended-spectrum beta-lactamase. Mortality due to NI was 10% in PICUs and 17% in neonatal units. We found large differences in NI frequency and microbial epidemiology in this European study. Viruses were the main pathogens in general pediatrics units. Catheter-related sepsis and CNS were frequent in newborns. A high frequency of multiresistant bacteria was observed in some units. Clinical monitoring of NIs and bacterial resistance profiles are required in all pediatric units.
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              Endotoxin and tumor necrosis factor challenges in dogs simulate the cardiovascular profile of human septic shock

              Survivors of both human and animal bacterial shock develop a characteristic pattern of progressive changes in cardiovascular function over a period of 7-10 d. In this present study, we examined whether endotoxin (a product of Gram-negative bacteria) or TNF (a cytokine released from macrophages) could reproduce the same complex cardiovascular changes observed in septic shock over a period of 7-10 d. To test this hypothesis, we implanted a thrombin-fibrin clot containing purified endotoxin from E. coli into the peritoneal cavity of eight dogs, and infused TNF into eight different dogs. Over the next 10 d, serial simultaneous heart scans and thermodilution cardiac outputs were performed in these awake nonsedated animals. By day 2 after challenge with either endotoxin or TNF, animals developed a decrease (p less than 0.05) in both mean arterial pressure and left ventricular ejection fraction. With fluid resuscitation, animals manifested left ventricular dilatation (increased [p less than 0.05] end diastolic volume index), increased or normal cardiac index, and decreased or normal systemic vascular resistance index. In surviving animals, these changes returned to normal with 7-10 d. The time course of these changes was concordant (p less than 0.05) with that previously described in a canine model of septic shock using viable bacteria. During the 10-d study, control animals receiving sterile clots or heat- inactivated TNF had not significant changes in hemodynamics. The results from this canine model demonstrate that either endotoxin or TNF alone can produce many of the same hemodynamic abnormalities seen in human septic shock and in a canine septic shock model induced by live bacteria. These findings support the hypothesis that the action of endogenous mediators (TNF) responding to bacterial products (endotoxin) is the common pathway that produces the serial cardiovascular changes found in septic shock.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                April 2006
                27 April 2006
                : 24
                : 3
                : 327-334
                aLife Science Research Laboratories, Life Science RD Center, Kaneka Corporation, Hyogo, and bResearch Group, Medical Devices Division, Kaneka Corporation, Osaka, Japan
                91997 Blood Purif 2006;24:327–334
                © 2006 S. Karger AG, Basel

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                Figures: 4, Tables: 2, References: 23, Pages: 8
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