sepsis/hypoxie

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Hypoxia inducible factor-1 alpha and prolinhydroxlase 2 polymorphisms in patients with severe sepsis: a prospective observational trial.

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Hypoxia-inducible-factor-1α (HIF-1α) and HIF-1 degrading prolyl-hydroxylases (PHD) are key regulators of the hypoxic-inflammatory response. Functionally active genetic variants in the HIF-1α (C/T; Single Nucleotide Polymorphism (SNP) rs11549465) and the PHD2 gene (EGLN1; C/T; SNP rs516651 and T/C;

Hypoxia in the term newborn: part three--sepsis and hypotension, neurologic, metabolic and hematologic disorders.

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Causes of hypoxia and cyanosis in the term newborn can be found within all physiologic systems and take the form of hundreds of specific diagnoses. In the first and second parts of this series, a wide range of cardiac and pulmonary causes for newborn hypoxia and cyanosis have been examined. Because

Evaluation of the role of cellular hypoxia in sepsis by the hypoxic marker [18F]fluoromisonidazole.

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Underlying cellular hypoxia, which may be difficult to detect, has been postulated to be a major cause of morbidity and mortality in sepsis. We employed the novel hypoxic marker [18F]fluoromisonidazole to determine whether cellular hypoxia was present in a peritonitis model of sepsis in the rat. A

Hypoxia-inducible factor and target gene expression are decreased in patients with sepsis: prospective observational clinical and cellular studies.

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BACKGROUND Hypoxia-inducible factor-1 (HIF-1) is a molecular key player in response to hypoxemic/inflammatory conditions prevailing in sepsis. In a prospective observational study, we tested the hypotheses that sepsis affects HIF-1α messenger ribonucleic acid (mRNA) expression (primary hypothesis)

A prospective multicenter cohort study of the association between global tissue hypoxia and coagulation abnormalities during early sepsis resuscitation.

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OBJECTIVE Coagulation activation is an integral part of sepsis pathogenesis. Experimental data suggest that endothelial exposure to hypoxia activates coagulation. We aimed to test the hypothesis that the quantity of exposure to global tissue hypoxia is associated with the degree of coagulation

[Diagnostic therapeutic problems of defibrination syndrome in shock, sepsis, and neonatal hypoxia (author's transl)].

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The diagnosis of defibrination syndrome in shock, sepsis and neonatal hypoxia is based, in addition to the clinical picture, upon a few parameters of the hemostatic system, which, in part as global tests, provide information about the course of coagulation. The parameters measured are partial

Effect of simvastatin on mitochondrial enzyme activities, ghrelin, hypoxia-inducible factor 1α in hepatic tissue during early phase of sepsis.

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We aimed to investigate the effects of prior treatment of simvastatin on mitochondrial enzyme, ghrelin, and hypoxia-inducible factor 1 α (HIF-1 α) on hepatic tissue in rats treated with Lipopolysaccharides (LPS) during the early phase of sepsis. Rats were divided into four groups: control, LPS (20

Tissue hypoxia during bacterial sepsis is attenuated by PR-39, an antibacterial peptide.

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Endotoxin (a lipopolysaccharide (LPS) component of the Gram negative bacterial cell wall) induces sepsis in laboratory animals and is the cause of septic shock in patients. Tissues often develop necrotic regions, particularly in kidney and liver, thought to be directly the result of

Mitochondrial respiration after sepsis and prolonged hypoxia.

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Recently, marked oxygen dependence of respiration by isolated mitochondria after exposure to prolonged hypoxia has been described. Because mitochondrial oxygen-dependent respiration could significantly influence oxygen consumption during critical illness, we sought to confirm the oxygen-dependent

Hemostatic changes in neonates with anoxia and sepsis.

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Hemostatic profile (prothrombin time (PT), thrombin time (TT), kaolin cephalin clotting time (KCCT), plasma fibrinogen, serum fibrin/fibrinogen degradation products (FDP) and platelet counts) was examined in 153 neonates with birth anoxia and 86 with sepsis. Remarkable hemostatic alterations

[Role of hypoxia-inducible factor in immunometabolism of sepsis].

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Sepsis remains a global disease with high morbidity and mortality. The changes of immune cell metabolism are of great significance in the pathophysiology of sepsis. Hypoxia-inducible factor (HIF) is not only a major regulator of hypoxic adaptive response, but also plays an important role in

A myeloid hypoxia-inducible factor 1α-Krüppel-like factor 2 pathway regulates gram-positive endotoxin-mediated sepsis.

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Although gram-positive infections account for the majority of cases of sepsis, the molecular mechanisms underlying their effects remains poorly understood. We investigated how cell wall components of gram-positive bacteria contribute to the development of sepsis. Experimental observations derived

Hypothermia protects brain mitochondrial function from hypoxemia in a murine model of sepsis.

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Sepsis is commonly associated with brain dysfunction, but the underlying mechanisms remain unclear, although mitochondrial dysfunction and microvascular abnormalities have been implicated. We therefore assessed whether cerebral mitochondrial dysfunction during systemic endotoxemia in mice increased

Impact of Intermittent Hypoxia on Sepsis Outcomes in a Murine Model.

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Sleep apnea has been associated with a variety of diseases, but its impact on sepsis outcome remains unclear. This study investigated the effect of intermittent hypoxia [IH]-the principal feature of sleep apnea-on murine sepsis. 5-week-old male C57BL6 mice were assigned to groups receiving severe IH

Cytopathic hypoxia in sepsis: a true problem?

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It is increasingly apparent that organ dysfunction in sepsis is caused, at least in part, by an acquired intrinsic derangement in cellular oxidative adenosine triphosphate (ATP) production. We have termed this phenomenon "cytopathic hypoxia". Although several different but mutually compatible

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