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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-five cultures of group JK bacteria isolated from clinical specimens were characterized morphologically and biochemically. The microorganisms were isolated primarily from blood cultures. The bacterial cultures produced positive reactions when tested for catalase, Tween hydrolysis, and carbohydrate fermentation. Glucose and galactose were fermented by more than 90% of the organisms. Gas-liquid chromatography of trimethylsilyl derivatives of whole-cell hydrolysates of some of the group JK cultures yielded nearly identical elution profiles. The group JK microorganisms were susceptible to vancomycin but were resistant to most of the other 17 antimicrobial agents tested. A method is presented for differentiating the group JK microorganisms from other similar bacteria encountered in clinical specimens. Although these bacteria rarely occur in clinical specimens, they are capable of producing fatal infections (endocarditis and sepsis) in humans.
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PMID:Characterization and identification of 95 diphtheroid (group JK) cultures isolated from clinical specimens. 11 Aug 26

Excessive hydrogen peroxide (H2O2) generation appears to contribute to the development of the adult respiratory distress syndrome (ARDS), but H2O2-combatting antioxidant defenses have not been evaluated. We found that serum from septic patients with ARDS scavenged more (p less than 0.05) H2O2 in vitro (82.7 +/- 3.8%) than did serum from septic patients without ARDS (56.9 +/- 3.1%) or control subjects (20.2 +/- 2.4%). Serum from septic patients with ARDS also had more (p less than 0.05) catalase activity (54.9 +/- 10.9 U/ml) than did serum from septic patients without ARDS (28.6 +/- 3.4 U/ml) or control subjects (7.3 +/- 0.8 U/ml). In contrast, serum from septic patients with or without ARDS and control subjects had the same glutathione peroxidase (GPX) activity. Serum H2O2 scavenging activity correlated with serum catalase (r = 0.77) but not GPX (r = 0.33) activity and was inhibitable (greater than 90%) by sodium azide, a catalase inhibitor. Increases in serum catalase activity did not appear to be derived from erythrocytes (RBC) because septic patients with or without ARDS and control subjects had similar RBC hemolysis in response to osmotic stress in vitro and serum haptoglobin concentrations. Serum from septic patients with ARDS also protected endothelial cells against H2O2-mediated damage (34.5 +/- 2.2% 51Cr release) better (p less than 0.05) than serum from septic patients without ARDS (47.3 +/- 7.4%) or control subjects (82.1 +/- 10.2%), but killing of bacteria by neutrophils in vitro was the same in serum from patients and control subjects. Our findings indicate that patients with sepsis and/or ARDS have increased serum catalase activity, which may alter H2O2-dependent processes.
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PMID:Increased serum catalase activity in septic patients with the adult respiratory distress syndrome. 141 29

The placement of rubber band tourniquets upon rat hind-limbs for 5 h followed by reperfusion of the extremities results in a severe form of circulatory shock characterized by hypotension and death within 24 h of tourniquet release. Oxidative damage to muscle tissue is an early consequence of hind-limb reperfusion on tourniquet release, yet this local damage does not explain the lethal hypotensive shock state which evolves within the next 24 h. Multiple system organ failure (MSOF), of as of yet unknown causes, is usually described in relation to several shock states. It has been suggested that injured or necrotic tissue may activate neutrophils, platelets, and the coagulation system leading to embolization in remote tissues. Effective decreases in hepatic blood flow have been observed in several forms of sepsis which precedes the biochemical evidence consistent with an ischemic insult of the liver. In support of our original hypothesis, that organ failure has its genesis in a primary perfusion abnormality with secondary ischemic organ injury, herein we have assessed the possibility that oxygen-derived free radicals are generated in the liver of rats after reperfusion of their hind-limbs on release of the tourniquets. We report on the protective effects of allopurinol (ALLO) and a mixture of superoxide dismutase (SOD) catalase (CAT) and dimethylsulfoxide (DMSO) on liver free sulfhydryl content (SH), thiobarbituric acid-reactive substances (TBARS), and on the release of aspartic acid (AsT) and alanine aminotransferase (AlT) activities, and of alkaline phosphatase during a 5 h tourniquet period and after 2 h of reperfusion of the hind-limbs. During the hind-limb ischemic period hepatis tissue SH levels remained essentially constant during the first hour (6.02 +/- 0.36 to 5.65 +/- 0.20 mumoles/g wet tissue), and decreased significantly, over and above the normal circadian decrease of liver glutathione levels, to 4.02 +/- 0.69 mumoles/g wet tissue after the third hour and remained lowered until tourniquet release. A further significant decrease (3.11 +/- 0.49 mumoles/g wet tissue) was observed after 2h of reperfusion. TBARS production remained constant during the 5 h hind-limb ischemic period (168.4 +/- 37.3 mumoles/g wet tissue) and rose by 55% to 261.7 +/- 55.8 mumoles/g wet tissue after 2 h of tourniquet release. ALLO, but not the SOD-CAT-DMSO combination, protected hepatic SH loss during the hind-limb ischemic insult, yet both offered protection after 2 h of tourniquet release.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxygen-derived free radicals mediate liver damage in rats subjected to tourniquet shock. 148 82

Twenty-nine vascular complications which occurred after 388 hepatic transplantations performed over a 5 year period (14 arterial thromboses, 4 aneurysms and ruptures of the hepatic artery, 8 portal thromboses and 3 peri-anastomosis portal stenoses) were investigated retrospectively in order to determine the role of imagery in diagnosing these vascular complications. The best screening examination for the diagnosis of hepatic artery thrombosis appeared to be pulsed Doppler coupled with echography. It provides a means of selecting candidates for arteriography, the only investigation allowing certain diagnosis of thrombosis. False aneurysms, suspected in cases of severe post-operative sepsis should be investigated with arteriography even if CAT scans and echo-pulsed Doppler imagery is normal. The diagnosis of portal thrombosis and stenosis relies on echo-pulsed Doppler imagery. In these cases, arteriography is carried out before treatment to evaluate the extent of vascular involvement. Thus echography coupled with pulsed Doppler is the best first intention screening examination to be performed whenever a vascular complication is suspected after hepatic transplantation. Nevertheless, arteriography remains the key examination for the diagnosis and evaluation of these complications.
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PMID:[Imaging in the diagnosis of vascular complications after hepatic transplantation]. 188 Jul 83

This work uses cecal perforation on the rat as a model of intra-abdominal sepsis. Under these conditions, various antibiotics were tested alone or in association with free radical scavengers, such as allopurinol and catalase. It can be concluded that the scavengers were not effective alone, but when combined with antibiotics they rendered good results in the majority of the groups when given postsepsis. Further studies are needed to determine the real role of agents like the free radical scavengers in infectious situations such as the one discussed here.
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PMID:Peritonitis after cecal perforation. An experimental model to study the therapeutic role of antibiotics associated with allopurinol and catalase. 203 30

Gram-negative bacterial sepsis is frequently associated with acute renal failure but the specific effects of lipopolysaccharide (LPS) and other bacterial products on kidney function are not known. Since either LPS or formyl-methionyl-leucyl-phenylalanine (FMLP)--a chemotactic peptide from bacterial cell walls--activate neutrophils (PMN) to release a number of potentially toxic factors in vitro, we determined the effect of adding PMN with LPS and/or FMLP to isolated perfused rat kidneys. Isolated rat kidneys perfused with LPS alone or LPS and normal PMN had normal glomerular filtration rates (GFR) and tubular Na reabsorption (TNa). Kidneys perfused with FMLP alone or FMLP and normal PMN also had normal GFR and TNa. In contrast, addition of PMN with both FMLP and LPS caused progressive renal dysfunction. For example, after 60 minutes of perfusion, GFR was reduced from 610 +/- 31 to 147 +/- 17 microliters/min/g and TNa from 97 +/- 1 to 72 +/- 2%, both P less than 0.01. Perfusion with the O2 metabolite scavengers catalase or dimethylthiourea afforded no protection while perfusion with the neutrophil elastase inhibitor Eglin C conferred substantial, but not complete, protection: GFR 492 +/- 34 microliters/min/g; TNa 91 +/- 3%. However, perfusion with both Eglin C and catalase completely prevented the toxic effects of LPS and FMLP-treated PMN on renal function. We conclude that in isolated kidneys, 1) the toxic effects of LPS requires FMLP-treated PMN and that 2) LPS and FMLP treated PMN cause progressive renal injury which is mediated by both O2 metabolites and neutrophil elastase.
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PMID:Role of neutrophil derived oxidants and elastase in lipopolysaccharide-mediated renal injury. 205 18

Live E. coli were infused i.v. in cats to induce gastrointestinal mucosal injury and the gastric mucosa was exposed to bile and a luminal pH of 1. A gastric lesion index was calculated and intestinal injury was graded. The effects of i.v. methylprednisolone before and after induction of bacteremia were compared with those of intragastric misoprostol combined with i.v. superoxide dismutase (SOD) and catalase and with a control group. Methylprednisolone, but not misoprostol/SOD/catalase, significantly reduced the gastric lesion index (p less than 0.05). The duodenum/small intestine was significantly injured in 4/6, 2/6 and 4/6 cats in the misoprostol/SOD/catalase, methylprednisolone and control groups, respectively (NS). End gastric luminal pH was 3.9, 2.7 and 4.5 in the respective groups (p less than 0.05), with systemic arterial pH 7.15, 7.15 and 7.32 (NS). Mean arterial pressure and cardiac output were improved with methylprednisolone. Misoprostol/SOD/catalase reduced late hypotension. Pulmonary arterial pressure rose to c. 200% of basal in all groups. Methylprednisolone, but not misoprostol/SOD/catalase, thus protected the gastric mucosa from sepsis-induced gastric injury concomitant with reduced disappearance of protons from the gastric lumen, but did not significantly affect small-bowel damage. Hemodynamic responses were significantly improved in methylprednisolone-pretreated cats.
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PMID:Feline E. coli bacteremia--effects of misoprostol/scavengers or methylprednisolone on hemodynamic reactions and gastrointestinal mucosal injury. 211 Jul 10

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest hereditary nephropathy. We collected 92 cases in VGH. Diagnosis was confirmed by intravenous pyelogram, renal sonogram, or renal CAT scan. The incidence of having positive family history was just only 28.3%. Patients were diagnosed at the mean age of 54 +/- 11 years (26-74 years). The common clinical findings were hypertension (73.9%), abdominal mass, proteinuria, anemia, azotemia, abdominal or back pain and pyuria in orders. Hypertension might present in the early stage with normal renal function (near 40%). Polycystic liver was the major extrarenal lesion (57.6%), but the incidence of abnormal liver function was only 10.1%. Enlarged kidneys were not always palpable, even at end stage of renal function (mean age 56 +/- 9 years, 89.4% kidney palpable). Patient's urine amount was usually nonoliguric, even in uremic stage (82.9%). Sepsis was the first cause of death. Cardiovascular disease and uremia were followed in sequence. Their expired mean age was 61 +/- 7 years (53-74 years).
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PMID:[Autosomal dominant polycystic kidney disease clinical analysis in VGH--Taipei]. 217 45

The myeloperoxidase-hydrogen peroxide-chloride (MPO-H2O2-Cl) system is an antimicrobial system of polymorphonuclear leukocytes. We demonstrated that the MPO-H2O2-Cl system is fungicidal for Trichophyton rubrum. Fungal growth of a synchronous cell culture of T. rubrum germlings was assayed by measuring the uptake of tritiated N-acetyl-D-glucosamine, and the viability of the fungi was assayed by counting colony-forming units. Cytotoxins produced by the interaction of myeloperoxidase with hydrogen peroxide and chloride ion were fungicidal for T. rubrum. Growth inhibition was abolished in the presence of catalase or L-methionine. Polymorphonuclear leukocytes through the MPO-H2O2-Cl system may prevent invasion and sepsis by dermatophytes even in the absence of specific immunity.
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PMID:Inhibition of growth of Trichophyton rubrum by the myeloperoxidase-hydrogen peroxide-chloride system. 253 15

To determine the susceptibility to sepsis in newborn infants deficient in glucose-6-phosphate dehydrogenase (G6PD), we screened 33,943 Saudi Arab infants. Deficiency of G6PD was found in 18%. Sepsis was determined by the presence of clinical signs of sepsis and confirmed by positive blood cultures. Sepsis was documented in 75 infants (2.2/1000). The incidence of sepsis was significantly higher in 6138 G6PD-deficient infants (3.4/1000) than in the 27,805 with normal G6PD activity (1.9/1000; p less than 0.02). The incidence of catalase-positive organism sepsis was higher in G6PD-deficient infants (2.9/1000) compared with those with normal G6PD activity (1/1000; p less than 0.0002), whereas the incidence of catalase-negative organism sepsis did not differ (p less than 0.2). Deficiency of G6PD was more common in infants with late sepsis (46%) than in those with early sepsis (21%) and in all infants screened (18%) (p less than 0.03 and p less than 0.001, respectively). We conclude that neonates with G6PD deficiency are more susceptible to late sepsis and to infection with catalase-positive organisms. The exact mechanism for the increased susceptibility is not clear, but a partial explanation could be lack of leukocyte bactericidal activity associated with G6PD deficiency, and an increased susceptibility to infection caused by hyperferremia resulting from lysis of G6PD-deficient erythrocytes.
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PMID:Incidence and causes of sepsis in glucose-6-phosphate dehydrogenase-deficient newborn infants. 271 88


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