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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion molecules play a critical role in the interaction of circulating neutrophils with vascular endothelium during inflammation. Increased quantities of soluble, circulating intercellular adhesion molecule-1 (cICAM-1) are present in various inflammatory conditions. The purpose of this investigation was to measure cICAM-1 levels in septic adults, as well as to examine the relationship between this potential marker of endothelial-cell activation and the consequences of sepsis (i.e., multiple organ failure and death). Using a sandwich-type enzyme-linked immunosorbent assay (ELISA), we measured cICAM-1 in blood samples obtained within 12 h of admission to an intensive care unit (ICU) for sepsis and other conditions. We found cICAM-1 levels to be increased in 25 septic patients (1,259 +/- 159 ng/ml, mean +/- SEM) as compared with 12 healthy volunteers (355 +/- 41 ng/ml, p < 0.0001) and four ICU patients without systemic inflammatory response syndrome (SIRS) (585 +/- 76 ng/ml, p < 0.001). Twenty-five patients with SIRS but no evidence of causative infection also had elevated levels of cICAM-1 (937 +/- 144 ng/ml, p = 0.12 versus sepsis). Serial measurements over the first week of sepsis demonstrated persistent elevation in most patients. Day 1 cICAM-1 levels were higher (p = 0.017, ANOVA) in 16 patients with septic shock than in seven with severe sepsis and two with sepsis but without hypotension or hypoperfusion. There was a positive correlation (r = 0.50, p = 0.009) between Day-1 cICAM-1 measurements and severity of shock as determined by the presence of hypotension and vasopressor use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating ICAM-1 is increased in septic shock. 773 95

Triglyceride-rich lipoproteins bind and inactive bacterial endotoxin in vitro and prevent death when given before a lethal dose of endotoxin in animals. However, lipoproteins have not yet been demonstrated to improve survival in polymicrobial gram-negative sepsis. We therefore tested the ability of triglyceride-rich lipoproteins to prevent death after cecal ligation and puncture (CLP) in rats. Animals were given bolus infusions of either chylomicrons (1 g triglyceride/kg per 4 h) or an equal volume of saline for 28 h after CLP. Chylomicron infusions significantly improved survival (measured at 96 h) compared with saline controls (80 vs 27%, P < or = 0.03). Chylomicron infusions also reduced serum levels of endotoxin, measured 90 min (26 +/- 3 vs 136 +/- 51 pg/ml, mean +/- SEM, P < or = 0.03) and 6 h (121 +/- 54 vs 1,026 +/- 459 pg/ml, P < or = 0.05) after CLP. The reduction in serum endotoxin correlated with a reduction in serum tumor necrosis factor, measured 6 h after CLP (0 +/- 0 vs 58 +/- 24 pg/ml, P < or = 0.03), suggesting that chylomicrons improve survival in this model by limiting macrophage exposure to endotoxin and thereby reducing secretion of inflammatory cytokines. Infusions of a synthetic triglyceride-rich lipid emulsion (Intralipid; KabiVitrum, Inc., Alameda, CA) (1 g triglyceride/kg) also significantly improved survival compared with saline controls (71 vs 27%, P < or = 0.03). These data demonstrate that triglyceride-rich lipoproteins can protect animals from lethal polymicrobial gram-negative sepsis.
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PMID:Triglyceride-rich lipoproteins prevent septic death in rats. 779 Aug 21

The present study was conducted to investigate changes in plasma membrane fluidity of the liver and kidney in sepsis, which is the main cause of multiple organ failure. Male Wistar rats weighing 200-250 g were used in all experiments. Sepsis was induced by cecal ligation and puncture. As a control, a sham operation was performed. The time course of plasma membrane fluidity of the liver and the renal cortex in septicemic rats or in controls was studied. To evaluate the fluidity, fluorescence polarization was measured using 1,6-diphenyl-1,3,5-hexatriene. The fluorescence polarization values of liver plasma membranes increased after cecal ligation and puncture: 0.183 +/- 0.004 (mean +/- SEM), 0.194 +/- 0.008, 0.206 +/- 0.003, and 0.210 +/- 0.002 at 0, 24, 48, and 72 hr, respectively. Corresponding values for membranes of the renal cortex increased in a similar fashion. To determine whether factors involved in cell membrane damage exist in blood, the direct effects of lipopolysaccharide (LPS), platelet-activating factor (PAF), and serum from normal rats or from septicemic rats on membrane fluidity were studied. The fluorescence polarization of plasma membranes of the liver or renal cortex to which septicemic rat serum was added was higher than that of plasma membranes to which normal rat serum was added. The fluorescence polarization of liver plasma membranes was increased by LPS, but that of plasma membranes of the renal cortex was slightly decreased. In addition, the fluorescence polarization of liver plasma membranes was increased by PAF, but that of plasma membranes of the renal cortex was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of altered fluidity of plasma membranes of the liver and kidney in rats with sepsis. 786 63

Endotoxin sensitivity varies among animal species and appears to correlate with the presence of pulmonary intravascular macrophage (PIM). In rats, which lack PIM, we investigated the hypothesis that chronic cholestatic liver injury leads to induction of PIM and endotoxin sensitivity. Rats were randomized to either common bile duct ligation (BDL) or sham-surgery and studied at 1 wk (acute cholestasis), 2 wk (cholestasis, early cirrhosis), and 4 wk (cholestasis, established cirrhosis) after surgery. Intravascularly injected fluorescent latex microspheres (1 micron diameter) were taken up by large phagocytic cells in lung parenchyma of BDL rats (at 2 and 4 wk), while no uptake was observed in lungs from control rats. Electronmicroscopy revealed accumulation of large, mononuclear, macrophage-like cells containing ingested latex particles within the pulmonary capillaries. Pulmonary intravascular phagocytosis, as reflected in lung uptake of 99mTc microaggregated albumin (Microlite, mean particle diameter = 1 micron), averaged 0.7 +/- 0.1% (mean +/- SEM) of total injected dose in 13 control rats and progressively increased with time after BDL (1 wk, 1.7 +/- 0.2%; 2 wk, 10.0 +/- 3.0%; 4 wk 35.1 +/- 5.9%). Rats with biliary cirrhosis were markedly sensitive to the lethal effects of low dose endotoxin and demonstrated marked lung edema at the time of death. Furthermore, the lung uptake of intravascular 125I-lipopolysaccharide was increased five-fold in cirrhotic rats. We conclude that chronic biliary obstruction leads to the induction of pulmonary intravascular phagocytes and enhances endotoxin sensitivity in rats. Pulmonary intravascular phagocytosis in patients with advanced cirrhosis may account for their increased susceptibility to sepsis-induced adult respiratory distress syndrome.
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PMID:Chronic biliary obstruction induces pulmonary intravascular phagocytosis and endotoxin sensitivity in rats. 796 47

Proctocolectomy with ileal pouch-anal anastomosis (IPAA) has become the procedure of choice for many children with ulcerative colitis and familial polyposis. The modified quadruple-limb (W) IPAA was designed to increase reservoir compliance and capacity, and to improve functional results by decreasing stool frequency. However, only limited information has been reported concerning the technical considerations and functional outcomes from W IPAA modification and utilization in the pediatric population. Additionally, pediatric IPAA physiological adaptation, expressed as IPAA volume/pressure relationships, for any type of IPAA design has not been described. In this report, the authors analyze their functional and physiological results with W IPAA in 19 children undergoing colectomy for ulcerative colitis and familial polyposis. Since 1986, 19 children (5 girls, 14 boys; mean age, 15.3 years [range, 11 to 18 years]) have undergone proctocolectomy with W IPAA for ulcerative colitis (n = 9) and familial polyposis (n = 10). IPAA pressure and volume profiles were measured in 10 patients at 2 and 12 months postileostomy takedown, and in five patients at 3 years. W IPAA compliance was calculated as the change in volume over change in pressure (delta V/delta P). There were no deaths, anastomotic leaks, or pelvic sepsis. The 24-hour stool frequency (mean +/- SEM) decreased significantly (P < or = .05) from 4.6 +/- 0.6 at 2 months to 3.3 +/- 0.1 at 12 months. No nighttime evacuation occurred after 12 months. W IPAA evacuation volume significantly increased (P < or = .05) from 238 +/- 22.9 mL at 2 months to 346 +/- 26.5 mL at 12 months and remained stable thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proctocolectomy and quadruple-limb W pouch reconstruction for the management of pediatric ulcerative colitis and familial polyposis. 801 4

We have studied 82 consecutive intensive care nursery admissions to determine rates of colonization and incidence of fungal sepsis. Cultures were obtained from stool, gastric aspirate and skin at three different times. Infants studied ranged in gestational age from 23 to 38 weeks (mean +/- SEM 29 +/- 0.4 weeks). Nineteen percent of all infants were colonized with Candida sp.; stools were more frequently culture-positive than skin or gastric aspirates. Colonized infants began enteral feeds at a later time compared with noncolonized neonates. Five of the study infants developed fungal sepsis. One had congenital Candida albicans sepsis and died at 10 days of age; the other four had Candida parapsilosis sepsis and survived. The development of C. parapsilosis sepsis was significantly associated with gastrointestinal colonization. Our results suggest that early initiation of enteral feeds decreases gastrointestinal colonization with C. parapsilosis. Gastrointestinal colonization was strongly associated with the subsequent development of C. parapsilosis sepsis in this group of high risk neonates.
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PMID:Incidence of Candida parapsilosis colonization in an intensive care nursery population and its association with invasive fungal disease. 807 41

It has been suggested that major surgery induces polymorphonuclear leukocyte (PMNL) dysfunction, which exposes patients to the development of sepsis. Conversely, the sepsis response and multisystem organ failure in patients after surgery is thought to be mediated by activated PMNLs. In a preliminary attempt to investigate this paradox, we studied functional (hydrogen peroxide production) and phenotypic (the adhesion/complement receptor CD11b) markers of PMNL activation in 28 patients undergoing elective major resectional surgery; 11 (39%) of these patients developed postoperative sepsis (the septic group). The mean (SEM) preoperative level of neutrophil CD11b expression (97.8 [6.2] mean channel fluorescence [MCF] and 101.42 [7.9] MCF; P = .74) and hydrogen peroxide production (109.51 [4.91] MCF and 104.53 [6.3] MCF; P = .5) were similar for the uncomplicated and septic groups, respectively. However, on the first postoperative day, both mean CD11b expression and hydrogen peroxide production were greater in those patients who subsequently developed postoperative sepsis (192.5 [38] MCF vs 128.6 [8.1] MCF for the septic group vs the uncomplicated group, respectively [P < .05], and 120.43 [2.56] MCF vs 109.61 [3.05] MCF for the septic group vs the uncomplicated group, respectively [P < .0001]). We suggest that an exaggerated PMNL activation response to surgery is an early event in those patients destined to develop postsurgical sepsis.
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PMID:Polymorphonuclear leukocyte activation. An early marker of the postsurgical sepsis response. 809 29

In order to identify a critical or an optimal therapeutic value for oxygen delivery and oxygen uptake, we analysed data from 40 publications concerning the relationship between oxygen delivery and consumption in patients with adult respiratory distress syndrome, trauma or during sepsis, and in nonseptic controls. According to the outcome, the patients were allocated to either group 1 (survivors) or group 2 (nonsurvivors). While oxygen delivery and uptake (mean, SEM) were significantly higher in patients with adult respiratory distress syndrome (636, SEM 31 ml.min-1.m-2 and 155, SEM 5 ml.min-1.m-2), trauma (782, SEM 77 ml.min-1.m-2 and 167, SEM 10 ml.min-1.m-2) and sepsis (654, SEM 28 ml.min-1.m-2 and 163, SEM 5 ml.min-1.m-2) than in nonseptic controls (452, SEM 18 ml.min-1.m-2 and 126, SEM 3 ml.min-1.m-2, p < 0.05), there were no significant differences in these parameters between survivors and nonsurvivors. Although therapeutic manoeuvres were effective in increasing both oxygen delivery and consumption, these improvements were not paralleled by an increase in survival rate. The correlation between oxygen delivery and uptake is generally a result of the use of pooled data and therefore prone to mathematical coupling. This is true particularly for patients with adult respiratory distress syndrome and sepsis. Thus, our study failed to identify either an optimal or a critical value of oxygen delivery or oxygen consumption in critically ill patients.
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PMID:The relationship between oxygen delivery and uptake in the critically ill: is there a critical or optimal therapeutic value? A meta-analysis. 814 18

Macrophage major histocompatibility complex (MHC) class II antigen expression is associated with defective antigen presentation to T lymphocytes in animals and is predictive of patient outcome after major trauma or sepsis. In this study, class II antigen (HLA-DR and DQ) expression on peripheral blood monocytes was investigated in patients with inflammatory bowel disease in relation to disease activity and outcome. The percentage positivity and fluorescent intensity of expression of HLA-DR and DQ antigens on monocytes were determined in whole blood samples using dual colour immunofluorescence labelling and flow cytometry. Disease activity was assessed using clinical and laboratory indices. There was no significant difference in percentage positivity or fluorescent intensity of class II antigen expression between patients with Crohn's disease, those with ulcerative colitis, and healthy volunteers. The percentage of monocytes displaying HLA-DR positivity was significantly decreased in patients with active ulcerative colitis (active %: 49.5 (5.6); inactive %: 78.9 (6.9); p = 0.01). Data expressed as mean (SEM). In patients requiring surgical resection of diseased bowel, the percentage of monocytes displaying HLA-DR positivity (51.9 (4.0) %) was significantly reduced compared with patients receiving medical treatment alone (81.1 (3.5) %; p < 0.001). Reduced monocyte HLA-DR expression is therefore associated with disease activity and seems to predict outcome in patients with inflammatory bowel disease.
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PMID:Class II major histocompatibility complex antigen expression on peripheral blood monocytes in patients with inflammatory bowel disease. 817 90

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26


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