Articles: sepsis.
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Comparative Study
Local beneficial effect of coumarin in experimental peritonitis.
Coumarin, a potent immune stimulant and macrophage activator, has been used to treat brucellosis and as an immune suppressor. The effect of Coumarin and systemic antibiotics on septicaemia, survival and peritoneal contamination in experimental peritonitis was assessed. Four groups of male Sprague-Dawley rats were inoculated with Clostridium perfringens, Escherichia coli and Bacteroides fragilis. ⋯ Coumarin did not improve survival whether given alone or in combination with antibiotics. Animals given Coumarin (Groups B and D) had significantly less peritoneal soiling (54%, 0%) (P less than 0.02, P less than 0.001) than their controls (Groups A and C: 92%; 29%). While Coumarin did not improve resistance to septicaemia it did exert a local beneficial effect.
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The rationale for the use of spinal cord stimulation (SCS) in the treatment of chronic pain arose from Melzack and Wall's gate theory of the control of pain (1965). Originally electrodes were placed directly on the spinal cord via open operation, while now they are placed by means of direct puncture the epidural space. ⋯ The implantation of an SCS system is a surgical procedure, which requires the highest standards in asepsis. The operation and its complications and ways of avoiding them are described.
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The production by monocytes of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF alpha) in intensive care unit (ICU) patients with sepsis syndrome (n = 23) or noninfectious shock (n = 6) is reported. Plasma cytokines, cell-associated cytokines within freshly isolated monocytes and LPS-induced in vitro cytokine production were assessed at admission and at regular intervals during ICU stay. TNF alpha and IL-6 were the most frequently detected circulating cytokines. ⋯ This reduced LPS-induced production of cytokines was most pronounced in patients with gram-negative infections. Finally, monocytes from survival patients, but not from nonsurvival ones recovered their capacity to produce normal amounts of cytokines upon LPS stimulation. In conclusion, our data indicate an in vivo activation of circulating monocytes during sepsis as well as in noninfectious shock and suggest that complex regulatory mechanisms can downregulate the production of cytokines by monocytes during severe infections.
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Because of the potential importance of interleukin 1 (IL-1) in modulating inflammation and the observations that human blood neutrophils (PMN) express IL-1 receptors (IL-1R) and synthesize IL-1 alpha and IL-1 beta, we studied the IL-1R on blood PMN from a group of patients with the sepsis syndrome. We report a marked enhancement in the sites per cell of IL-1R expressed on sepsis-PMN of 25 consecutively studied patients compared to 20 controls (patient mean = 9,329 +/- 2,212 SE; control mean = 716 +/- 42 SE, respectively). There was no demonstrable difference in the Kd of IL-1R on sepsis-PMN (approximately 1 nM) as determined by saturation curves of 125I-IL-1 alpha binding and the IL-1R on sepsis-PMN had an apparent Mr approximately 68,000, a value like that of normal PMN. ⋯ Similar increases in expression of IL-1R were not observed in various other inflammatory processes, including acute disseminated inflammation and organ failure not caused by infection, acute infection without organ failure, and immunopathologies such as active systemic lupus erythematosus and rheumatoid arthritis. Enhanced expression of IL-1R was not related simply to the state of myeloid stimulation. Increased expression of IL-1R on normal PMN was induced in vitro by incubating cells with recombinant human granulocyte-macrophage/colony-stimulating factor for 18 h and this response was inhibited by cycloheximide, suggesting the possibility that de novo synthesis of IL-1R might occur in PMN during the sepsis syndrome.