Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary microvascular injury during sepsis after injury appears to be amplified with plasma fibronectin deficiency, but the degree of injury relative to the extent of sepsis has not been defined. We evaluated pulmonary vascular permeability in sheep as influenced by various levels of postoperative Pseudomonas sepsis during a period of plasma fibronectin deficiency. The hemodynamic response to Pseudomonas was very similar regardless of the intensity of septic challenge and characterized by systemic arterial hypotension, decreased cardiac output, and pulmonary arterial hypertension. In contrast, increased pulmonary microvascular permeability was observed with increments in the bacterial challenge. Thus, lung protein clearance (LPC) or so called pulmonary transvascular protein clearance (TPC) used as an index of lung vascular permeability was 9.1 +/- 1.9 ml/hr, 15.1 +/- 1.7 ml/hr, and 19.3 +/- 3.0 ml/hr 2 hr after low (3 X 10(9) i.v.; 1 X 10(10) i.p.), medium (3 X 10(9) i.v.; 3 X 10(10) i.p.), and high (5 X 10(9) i.v.; 5 X 10(10) i.p.) dose Pseudomonas challenges, respectively. Thus, the extent of the altered pulmonary microvascular integrity in sheep during sepsis after surgery in the presence of fibronectin deficiency is dependent on the degree of bacterial sepsis. In addition, infusion of cryoprecipitate was an effective means of reversing the plasma fibronectin deficiency. Accordingly, this may be used as a model to investigate the mechanism of altered lung fluid balance during postoperative septic shock and the effect of fibronectin on this response.
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PMID:Lung fluid and protein flux during postoperative sepsis. 405 99

Plasma fibronectin (pFN) levels were measured in 52 patients throughout their stay in an intensive care unit. At the same time a close watch was kept for signs of sepsis. Low pFN levels regularly accompanied--but did not precede--infectious episodes and were also found in patients without septic complications. These findings indicate that a fall in pFN does not constitute a factor of increased susceptibility to infection.
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PMID:[Plasma fibronectin. Role in severe infections and intensive care]. 622 Dec 83

Plasma fibronectin (PFN) depletion has been associated with poor outcome in patients with sepsis or those who have experienced trauma; restoration of normal levels appears beneficial. PFN synthesis is increased after cecal ligation even in malnourished animals with sepsis, implying that stimulation of endogenous PFN synthesis is possible. One hundred rats received either a single therapeutic agent (gelatin, heparin, indomethacin, urokinase, captopril, or endotoxin) or the combination of a cecal ligation and a single agent (cimetidine, methylprednisolone, epsilon-aminocaproic acid (EACA), or transaminomethyl cyclohexane carboxylic acid. PFN levels were measured by enzyme-linked immunosorbent assay at 0, 24, and 48 hours. Only endotoxin alone caused significant PFN elevation at 24 to 48 hours (p less than 0.01); however, its multiplicity of effects precludes localization of regulatory pathways. Methylprednisolone results in an accelerated rise in PFN levels after operation (p less than 0.05), probably through an intracellular augmentation PFN synthesis. EACA attenuates the postoperative response while transaminomethyl cyclohexane carboxylic acid augments the PFN rise. This effect of EACA implies the existence of a proteolytic fragment capable of stimulating PFN synthesis. If a nontoxic factor can be identified, the use of exogenous PFN may be avoided.
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PMID:Modulators of plasma fibronectin response during sepsis. 637 57

Fibronectin (FN) is a glycoprotein (disulfite-bonded dimer of 200 to 220 Kd submits) found in a soluble form in blood (concentration 250--500 microg/ml), it can be removed from it by cryoprecipitation and affinity chromatography on gelatin or heparin-agarose. It is also found in an insoluble fibrillar form as a component of connective tissue matrix like collagen, proteoglycans... FN fundamentally forms molecular complexes with collagen, fibrinogen or fibrin, heparin, activated factor XIII, bacteria, cellular membranes..., these various proteins binding with now well known functional "domains" on subunits. Thus FN mediates adhesion of cells to cells as well to biomaterials or tissue, cell migration and chemotactic activity, tissue stromal organization... The transformed cultured cells in presence of oncogen virus loose ability to secrete FN which contribute to their invasive tendency. FN also interacts with hemostatic and fibrinolytic systems, as component of the subendothelium (secreted, like Willbrand factor, by endothelial cells) and of platelet alpha-granules released by stimulated platelets. FN could then provoke platelet spreading on the subendothelium surface after collagen-platelet adhesion, triggered by Willebrand factor, has happened. FN is a part of the fibrinous clot. It participates in anchorage of the clot to subendothelium and mediates its colonisation by fibroblasts, first step to wound reparation. Lastly FN probably has an important role in organism defence. It acts as a non-immunological opsonin, promoting phagocytosis by RES macrophages of bacteria, cellular or fibrin fragments, immune complexes... present in blood. Plasmatic FN concentration is strongly decreased in several ill patients following major trauma, extensive burns, shock, sepsis, with or not evidence of DIVC, of respiratory distress... SABA and various other authors have obtained good results after injections of FN (as cryoprecipitates or concentrated fractions). It is yet necessary to confirm therapeutic role of FN.
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PMID:[Plasma fibronectin]. 641

Plasma fibronectin deficiency and opsonic dysfunction exist in critically ill septic surgical, trauma, and burn patients with multiple organ failure. Fibronectin deficiency can be reversed by infusion of fresh plasma cryoprecipitate. The influence of therapy with human cryoprecipitate on lung vascular permeability in septic sheep with plasma fibronectin deficiency following surgery was evaluated. Additionally, selected studies on pulmonary function in septic surgical and trauma patients after infusion of plasma cryoprecipitate were completed. In patients, ventilation-perfusion balance appeared to improve as measured by the multiple inert gas elimination technique. With the lung lymph fistula preparation in fibronectin deficient sheep, infusion of human plasma cryoprecipitate (10 units; 250 ml) delayed the onset and minimized the increase in lung vascular permeability during postoperative Pseudomonas sepsis (5 X 10(9) bacteria, I.V.; 5 X 10(10) bacteria, I.P.). For example, in a first group of sheep, the transvascular protein clearance (TPC) at 2 hrs in septic sheep (n = 4) treated with only saline (volume control) was 20.1 +/- 3.1 ml/hr, compared to 11.23 +/- 0.83 ml/hr in the sheep (n =a 4) treated with fibronectin-rich cryoprecipitate (p less than 0.05). In a second group of sheep, cryoprecipitate depleted of fibronectin by affinity chromatography was used as the control solution. It also did not manifest this protective effect with respect to lung vascular permeability. Thus, at 2 hrs the lymph flow (Qlym) was 30.2 ml/hr and the transvascular protein clearance (TPC) was 18.0 ml/hr in septic sheep given fibronectin-deficient cryoprecipitate. In contrast, in the fibronectin-rich cryoprecipitate treated sheep, the Qlym was 14.8 ml/hr and the TPC was 8.12 ml/hr. It is suggested that fibronectin may influence lung vascular integrity during sepsis following surgery and trauma.
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PMID:Lung vascular permeability after reversal of fibronectin deficiency in septic sheep. Correlation with patient studies. 641 92

Fibronectin levels were measured in 151 hospitalized patients with liver disease, sepsis, malignancy, leukemia, and following trauma or surgery, using heterologous precipitating antibody in an immunoassay. The mean (+/- S.E.M.) in 25 controls was 0.95 +/- 0.06 U/ml, with females, 0.83 +/- 0.07 U/ml, lower than males, 1.09 +/- 0.09 U/ml. Mean fibronectin levels were decreased in all disease groups except in obstructive liver disease. The reduced levels in hepatocellular disease and the restoration of levels to normal after orthotopic liver transplantation in patients with hepatocellular disease supports the theory that hepatic synthesis contributes significantly to plasma fibronectin levels. Following cryoprecipitate infusion in four hemophiliac patients, plasma fibronectin levels rose to 32% to 45% of the levels predicted. In patients with reduced fibronectin and poor clinical response to standard treatment (antibiotics, chemotherapy), cryoprecipitate infusions may raise the levels of fibronectin and, perhaps, contribute to clinical improvement.
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PMID:Plasma fibronectin levels in clinical disease states and after cryoprecipitate infusion. 644 71

Plasma fibronectin and a fragment of the third component of complement (C3b) are both opsonins of the reticulo-endothelial system. Twenty patients undergoing uncomplicated gastro-intestinal surgery were studied. There was a significant reduction in plasma fibronectin and total haemolytic complement, but not C3, in the early postoperative period (days 1 to 3). In six surgical patients critically ill with severe sepsis both plasma fibronectin concentrations and C3 concentration were reduced significantly when compared with the early postoperative period of uncomplicated surgery. In addition, in the critically ill patients, direct evidence of complement activation was demonstrated. These studies show a transient reduction of humoral host defence mechanisms following surgery which may be permissive to bacteraemia and complement activation.
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PMID:Plasma fibronectin and complement in surgical patients. 647 67

Plasma fibronectin concentrations were measured in 33 patients with major burn injury. Changes in plasma fibronectin concentration were related to the day of burn injury, surgery and to the development of sepsis. Within 24 hours of the burn injury and surgical treatment, a decrease of the plasma fibronectin concentration was observed, which returned to normal values within 72 hours. A decrease in the plasma fibronectin concentration was observed as sepsis developed, while recovery from septicaemia was associated with plasma fibronectin concentration returning to normal values.
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PMID:Plasma fibronectin concentrations in patients with severe burn injury. 647 89

Depletion of plasma fibronectin has been observed in certain clinical conditions predisposing to the adult respiratory distress syndrome and has been associated with cardiopulmonary dysfunction in experimental lung injury. We evaluated prospectively the relationship between plasma fibronectin concentration and the development of the adult respiratory distress syndrome in patients known to be at high risk. Although plasma fibronectin levels in participants at study entry were lower in this population (mean 258 +/- 132 micrograms/ml) than in normal volunteers (461 +/- 127 micrograms/ml, p less than 0.0025), there was no difference between patients who subsequently developed the adult distress syndrome (mean 255 +/- 149 micrograms/ml) and those with similar illness or injury who did not develop the syndrome (260 +/- 126 micrograms/ml). Fibronectin concentration was not further depressed even after development of adult respiratory distress syndrome and did not correlate with degree of pulmonary dysfunction. These data suggest that fibronectin depletion is not an important determinant of respiratory failure in humans. Patients with sepsis syndrome had significantly lower plasma fibronectin levels than those without sepsis (187 +/- 119 micrograms/ml vs. 273 +/- 131 micrograms/ml, p less than 0.05), suggesting a possible role for fibronectin in the pathogenesis of sepsis.
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PMID:Measurement of plasma fibronectin in patients who develop the adult respiratory distress syndrome. 648 Dec 18

Plasma fibronectin (PFN) is a high molecular weight adhesive glycoprotein. Following trauma or sepsis PFN is acutely depleted, with rapid restoration of normal or supranormal levels after 24 to 48 hours. Cecal ligation with perforation provides an animal model of surgical trauma combined with polymicrobial sepsis. The present study examines whether this PFN level restoration 6 to 24 hours postoperatively is associated with de novo PFN synthesis and how this response is altered by pre-existing protein-calorie deprivation. Thirty-six adult male rats were divided into four groups: I--Controls, II--Prefasted Controls, III--Ligated, IV--Prefasted and Ligated. Control and experimental groups received intracardiac 35S-methionine 2 hours postoperatively. Plasma fibronectin (PFN) levels, PFN specific activity, plasma total protein, and total protein specific activity were determined at 0, 6, 24, and 48 hours postoperatively. Ligated rats (Groups III & IV) demonstrated significant PFN level increases 24 to 48 hours postoperatively (p less than 0.01-0.05). Despite a significant preoperative PFN level depression in prefasted rats (Groups II & IV), the 24-48 hours response to cecal ligation was not significantly altered. PFN specific activity was significantly increased among the operative groups 6 hours postoperatively, demonstrating de novo PFN synthesis following cecal ligation and perforation.
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PMID:Plasma fibronectin response to sepsis: mobilization or synthesis? 648 33


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