Endotoxic Shock
Mostrando 1-12 de 71 artigos, teses e dissertações.
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1. Metabolismo de triptofano na vigência de choque endotóxico induzido por LPS e hipertriptofanemia / Metabolism of tryptophan in the presence of LPS-induced endotoxic shock and hypertryptofanemia
Triptofano (TRP), um amino ácido essencial, é metabolizado por duas vias principais, a via das quinureninas e a via serotonérgica. Em ambas as vias há a possibilidade de formação de compostos ativos no sistema imune que se caracterizam pelas ações imunossupressoras e indutoras de tolerância. Na via serotonérgica há a formação de serotonina (5-HT
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 15/12/2010
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2. Study of the involvement of acute inflammatory reaction loci in the determination of sensitivity or resistance to endotoxic shock induzed by LPS. / Estudo do envolvimento dos loci reguladores da reação inflamatória aguda na determinação da sensibilidade ou resistência ao choque endotóxico induzido por lipopolissacarídeo.
Linhagens de camundongos selecionadas para a máxima (AIRmax) ou mínima (AIRmin) resposta inflamatória aguda diferem tanto na susceptibilidade a infecção por Salmonella entérica sorotipo Typhimurium (S. Typhimurium) e ao LPS. Diferentes frequências dos alelos do gene Nramp1, envolvido na resistência inata a infecção por S. Typhimurium, foram encontr
Publicado em: 2009
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3. Efeitos do jejum agudo ou jejum intermitente na evolução da peritonite bacteriana induzida por ligadura e punção do ceco ou por injeção intra-peritoneal de suspensão fecal em camundongos / Efeitos do jejum agudo ou jejum intermitente na evolução da peritonite bacteriana induzida por ligadura e punção do ceco ou por injeção intra-peritoneal de suspensão fecal em camundongos
Intermittent fasting is frequent in medical practice and this condition has been studied as a therapeutic intervention for some diseases. Increased life span and resistance to stress is observed in rodents submitted to intermittent fasting. However there is not much information on the evolution of infections in animals submitted to these diet manipulations.
Publicado em: 2007
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4. Essential Role for Estrogen in Protection against Vibrio vulnificus-Induced Endotoxic Shock
Little is known about the underlying mechanisms that result in a sexually dimorphic response to Vibrio vulnificus endotoxic shock. V. vulnificus is a gram-negative bacterium, considered one of the most invasive and rapidly fatal human pathogens known. However, 85% of individuals that develop endotoxic shock from V. vulnificus are males. Using the rat, we hav
American Society for Microbiology.
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5. Multiple opioid receptors in endotoxic shock: evidence for delta involvement and mu-delta interactions in vivo.
The use of selective delta and mu opioid antagonists has provided evidence that delta opioid receptors within the brain mediate the endogenous opioid component of endotoxic shock hypotension. The selectivity of these delta and mu antagonists was demonstrated by their differing effects upon morphine analgesia and endotoxic hypotension. The mu antagonist beta-
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6. Endotoxin-induced pulmonary dysfunction is prevented by C1-esterase inhibitor.
In septic shock, hypotension, disseminated intravascular coagulation, and neutrophil activation are related to the activation of the blood coagulation contact system. This study evaluates in dogs the effect of the C1-esterase inhibitor (C1-INH), a main inhibitor of the blood coagulation contact system, on the cardiovascular and respiratory dysfunction associ
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7. Effects of Ibuprofen on the physiology and outcome of rabbit endotoxic shock
BioMed Central.
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8. Pretreatment of Mice with Clindamycin Improves Survival of Endotoxic Shock by Modulating the Release of Inflammatory Cytokines
Suppression of endotoxin release and subsequent production of inflammatory cytokines is crucial in the treatment of septic shock. We investigated the effect of clindamycin (CLI) on endotoxic shock induced in mice by Escherichia coli lipopolysaccharide (LPS). Mice were treated with CLI (160 to 600 mg/kg) or saline and then injected with E. coli LPS and d-(+)-
American Society for Microbiology.
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9. Targeting the ubiquitin proteasome pathway for the treatment of septic shock in patients
Endotoxic shock is a serious systemic inflammatory response to an external biological stressor. The responsiveness of NF-κB is built upon rapid protein modification and degradation involving the ubiquitin proteasome pathway. Using transgenic mice, we have obtained in vivo evidence that interference with this pathway can alleviate the symptoms of toxic shock
BioMed Central.
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10. Interleukin-10 is a central regulator of the response to LPS in murine models of endotoxic shock and the Shwartzman reaction but not endotoxin tolerance.
Previous studies in vivo have shown that IL-10 infusion can prevent lethal endotoxic shock. Mice deficient in the production of IL-10 (IL10T) were used to investigate the regulatory role of IL-10 in the responses to LPS in three experimental systems. In a model of acute endotoxic shock, it was found that the lethal dose of LPS for IL10T mice was 20-fold lowe
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11. Antiendotoxin activity of cationic peptide antimicrobial agents.
The endotoxin from gram-negative bacteria consists of a molecule lipopolysaccharide (LPS) which can be shed by bacteria during antimicrobial therapy. A resulting syndrome, endotoxic shock, is a leading cause of death in the developed world. Thus, there is great interest in the development of antimicrobial agents which can reverse rather than promote sepsis,
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12. Elevated Thromboxane Levels in the Rat during Endotoxic Shock: PROTECTIVE EFFECTS OF IMIDAZOLE, 13-AZAPROSTANOIC ACID, OR ESSENTIAL FATTY ACID DEFICIENCY
The potential deleterious role of the proaggregatory vasoconstrictor, thromboxane A2, in endotoxic shock was investigated in rats. Plasma thromboxane A2 was determined by radioimmunoassay of its stable metabolite thromboxane B2. After intravenous administration of Salmonella enteritidis endotoxin (20 mg/kg), plasma thromboxane B2 levels increased from nondet