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

The administration of a single mixture of the components of total parenteral nutrition (TPN) constitutes total nutritional admixture (TNA), the safety and efficacy of which in a variety of clinical settings have been confirmed by controlled trials. According to the nitrogen balance and stable isotope methods, TNA is as efficacious as the old system of three bottles with piggyback intravenous fat emulsion in maintaining body nitrogen mass, visceral protein, and liver function. Also, serum concentrations of electrolytes, trace elements, and vitamins can be maintained adequately using the TNA system. The other advantages are the timesaving to the nursing staff, with its hidden savings in cost; the avoidance of a peripheral catheter solely for the infusion of lipid emulsion in addition to the central catheter for TPN in hospitalized patients; and the facility of use in home nutrition programs. The ease of home use has resulted in a greater degree of patient compliance; thus patients receive a mixed-fuel system while avoiding the hazards of a piggyback infusion, with all its potential complications. Among the perceived disadvantages of TNA are a supposed higher frequency of catheter-related sepsis, a view based on in vitro studies that is not borne out by in vivo studies; catheter occlusion by precipitation of calcium salts; and enhanced ability to clear fat and thus fat tolerance with continuous infusion of lipids. Numerous studies have shown that these concerns are unwarranted.
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PMID:Clinical use of total nutritional admixtures. 213 56

Hemorrhage in patients with Lassa fever is associated with the presence of a circulating plasma inhibitor of platelet aggregation. This study was to determine whether patients with Argentine hemorrhagic fever (AHF) develop a similar inhibitor. Normal platelets showed significantly weaker aggregation responses to a sub-maximal dose of adenosine diphosphate (ADP) when mixed with plasma from 10 patients with AHF (mean percent of control +/- 1 SE = 57.2 +/- 6.7%) compared to those mixed with plasma from 9 viral control patients (79.5 +/- 4.1%; P less than 0.05) and 9 febrile patients with septicemia (103.8 +/- 3%; P less than 0.001). Plasma from 3 patients with severe AHF inhibited in a dose-dependent fashion the aggregation responses of normal platelets to collagen, sodium arachidonate, a calcium ionophore (A23187), and ristocetin; none of 4 samples from convalescent AHF patients showed this inhibitory activity. The platelet inhibition was sudden in onset and unaffected by a 30 min pre-incubation, not neutralized by convalescent plasma with high titer antibody to Junin virus, and abolished after heating plasma from an AHF patient at 56 degrees C for 30 min. Hemorrhage in AHF is associated with the presence of a circulating inhibitor of platelet aggregation, and disturbed hemostasis in arenavirus-induced hemorrhagic fevers may have a common basis.
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PMID:A plasma inhibitor of platelet aggregation in patients with Argentine hemorrhagic fever. 216 Jan 97

Despite numerous reports, the role of tumor necrosis factor (TNF) in polymorphonuclear leukocyte (PMN) function remains controversial. We found TNF to be a potent, pertussis toxin-independent stimulator of PMN adhesion (ED50 2.6 pM). TNF-stimulated PMN under adherent conditions released up to 65% of their transcobalamine content (ED50 3.9 pM) and increased their burst activity 10-fold (ED50 3.2 pM) as measured by the hexose monophosphate shunt, whereas PMN held in suspension hardly degranulated at all and only little burst activity was demonstrable. However, preincubation of PMN with TNF in suspension led to a decrease in cellular adhesiveness, degranulation, and burst activity in response to a secondary stimulus of TNF under adherent conditions, although cells remained fully responsive toward phorbol myristate acetate. A concomitant dose-dependent decline of TNF receptor numbers that correlated well with the inhibition of PMN function (r = 0.91) suggests receptor down-regulation as the mechanism of functional PMN deactivation. Remarkably, preincubation with other PMN stimuli such as N-formyl-methionyl-leucyl-phenylalanine, platelet-activating factor, leukotriene B4, complement component fragment 5a (C5a)/C5a (desarginated), and endotoxin also led to a reduction of TNF-specific PMN responses (cross-deactivation) from 35% (LTB4) to 90% (endotoxin), corresponding with the down-regulation of TNF receptors. Deactivation and receptor down-regulation are independent of pertussis toxin-sensitive G proteins and protein kinase C but seemed to depend on changes in calcium metabolism. Granulocyte hyporesponsiveness towards TNF in sepsis (with elevated blood levels of endotoxin and TNF) might be a mechanism of self-protection or, to the contrary, might impair a possibly central mode of host defense.
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PMID:The tumor necrosis factor receptor and human neutrophil function. Deactivation and cross-deactivation of tumor necrosis factor-induced neutrophil responses by receptor down-regulation. 216 42

Continuous i.v. infusion of a nonlethal dose of Escherichia coli endotoxin induced an early (3-h) accumulation of neutrophils in the rat liver followed by a later (30-h) greater extravasation of mononuclear phagocytes (MNP). These inflammatory cells, recovered together by centrifugal elutriation, were analyzed for their potential capacity to metabolize [1-14C]-AA. Ca2+ ionophore A23187 (5 microM) stimulated the release of [1-14C]-AA from PC and PI both in cells from saline- and ET-infused rats, the latter showing a higher capacity to further metabolize AA to eicosanoids. LTB4 and 5-HETE were the major metabolites accumulated in cells from rats infused with ET for 3 h, while PGD2 played the main role in cells from saline-infused rats. This could reflect [1-14C]-AA metabolism by PMNP and Kupffer cells, respectively. By 30 h of ET-infusion, a shift from PGD2 to PGE2 release was observed. These results suggest that eicosanoids released by nonparenchymal cells (i.e., Kupffer and endothelial cells) and PMNP in the liver of ET-infused rats may alter the normal intercellular information flow between parenchymal and nonparenchymal cells, contributing to the severe impairment in liver function and metabolism during endotoxicosis and sepsis.
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PMID:Eicosanoid production in nonparenchymal liver cells isolated from rats infused with E. coli endotoxin. 217 32

Ionized calcium is a physiologically critical calcium pool. It is easily determined, although accuracy depends on sample handling. As a clinical parameter, directly measured ionized calcium has particular import in the care of neonates, patients with sepsis or other cardiovascular instability, massively transfused patients, and those undergoing cardiopulmonary bypass or liver transplantation. Disturbances of calcium occur in many other settings, however, and accurate diagnosis and research conclusions may depend on using the best measurement available. Clinical and investigational use of ionized calcium determinations represent appropriate applications of current proven technology. In the future, clinical calcium manipulation may include modifying specific transmembrane transport processes and intracellular calcium pools and movements. At the current time we are largely restricted to studies of extracellular calcium concentration and its interactions. Much is known, but Mother Nature still has too many secrets. The interested reader is referred to discussions of ionized calcium and hemodynamics, reviews of the endocrine disturbances of calcium and phosphorus, textbook discussions pertinent to general calcium disturbances, and critical care issues.
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PMID:Ionized calcium: pediatric perspective. 218 3

Horses suffering from trauma, sepsis, and severe burns need 12% to 16% of protein (dry matter basis) in their diet. Since reduced appetite may be a problem, relatively energy dense (greater than 2 Mcal DE/kg) feeds should be offered. In hepatic failure, maintenance protein requirements (8% on a dry matter basis for adult horses) should be met with feeds that are high in short branched-chain amino acids and arginine but low in aromatic amino acids and tryptophan (for example, milo, corn, soybean, or linseed meal) in addition to grass hay. Vitamins A, C, and E should also be supplemented. In cases with renal failure, protein, calcium, and phosphorus should be restricted to maintenance or lower levels. Grass hay and corn are the best feeds for horses with reduced renal function. Do not offer free-choice salt to horses with dependent edema from uncompensated chronic heart failure. Following gastrointestinal resection, legume hay and grain mixtures are the feeds of choice. Horses with diarrhea should not be deprived or oral or enteral alimentation for prolonged periods of time. Liquid formulas may be used if bulk or gastrointestinal motility are a problem. Apple cider vinegar and a high grain diet may reduce the incidence of enteroliths in horses prone to this problem. Pelleted feeds will reduce fecal volume and produce softer feces for horses that have had rectovaginal lacerations or surgery. Horses with small intestinal dysfunction or resection should be offered low residue diets initially, but long-term maintenance requires diets that promote large intestinal digestion (alfalfa hay, vegetable oil, restricted grain). Geriatric horses (greater than 20 years old need diets similar to those recommended for horses 6 to 18 months old.
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PMID:Clinical nutrition of adult horses. 220 96

The involvement of the myocardium in the injury resulting from bacteremia has been somewhat controversial. Recently, some investigators have suggested that the transition from an early stage of sepsis, in which the cardiovascular system is stable and mortality is relatively low, to the late or preterminal stage of sepsis is a result of cardiac dysfunction. Here, however, data are presented to show that contractile defects and loss of myocardial reserve occur even early during a septic episode, i.e., at a time when cardiac output is elevated or normal. Efforts to determine the mechanism of the cardiac dysfunction are described. These entail studies of whole heart performance under conditions of varying the calcium availability for contraction and assessment of subcellular organelle function. The data indicate that calcium dyshomeostasis may at least partially contribute to the cardiac dysfunction of sepsis. The in vivo adequacy of cardiac function probably results from the capacity of the myocardium in early sepsis to respond to catecholamine support of chronotropy and inotropy.
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PMID:In vitro cardiac function in early sepsis. 221 67

From April 1984 to November 1989, 194 cases of neonatal hyperbilirubinemia treated with blood exchange transfusions (BET) were studied. The patients included 127 male and 67 female neonates, with an age ranged from 13 hours to 16 days. The most common cause was idiopathic (52.6%), followed by G-6-PD deficiency (23.7%), and sepsis (12.9%). Most of the neonates received BET at the 4th day of birth (23.2%), but there were still 30 cases (15.5%) that received BET after 1 week of age. There were 17 cases (8.8%) with maximum serum bilirubin lower than 20 mg/dl before receiving BET, five of them were LBW infants; 11 cases (5.7%) were greater than 40 mg/dl. The mean of maximum serum bilirubin was 26.9 +/- 7.96 mg/dl. Most of the cases received BET once (145 cases) or twice (33 cases). There were two cases that received up to six BET's. One was G-6-PD deficiency and one idiopathic in etiology. No significant difference of BET frequency between sex or body weight (p greater than 0.05) was found. Newborns with higher serum bilirubin due to G-6-PD deficiency, received more BET (p less than 0.05). No significant differences of the pH value (7.33 +/- 0.08 vs 7.35 +/- 0.10) and bicarbonate values (21.20 +/- 3.99 vs 22.00 +/- 3.83 mM/L) occurred before and after blood exchange transfusion (p greater than 0.1). The serum calcium decreased significantly after BET (3.88 +/- 0.91 vs 3.15 +/- 6.97 mEq/L, p less than 0.05). There were 11 deaths in this series, the mortality rate was 5.7%. Three cases (1.5%) were dead within 6 hours after BET.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical studies of neonatal hyperbilirubinemia treated with blood exchange transfusion]. 224 73

Decreased cytosolic [Ca2+] and impaired Ca2+ release in response to an IP3 challenge are among perturbations in hepatocyte Ca2+ homeostasis associated with endotoxemia and sepsis. These changes are consistent with the accompanying alterations in appropriate physiologic functions, e.g., activation of glycogen phosphorylase and gluconeogenesis, mediated by [Ca2+]c and defective phosphorylation of relevant enzymes. Attenuation of IP3 binding to the subcellular fractions that are imputed to be targets of IP3 and a decrease in the size of the IP3-sensitive pool of releasable Ca2+ are underlying components of the mechanism of the reduced Ca2+ release upon IP3 stimulation and its metabolic sequelae. ET treatment leads to a significant increase in Ca2+ associated with the cell surface compartment of adipocytes, a reduction in 45Ca2+ uptake by endoplasmic reticulum and higher cytosolic [Ca2+] under basal conditions and upon ACTH stimulation than that observed in cells of control rats. The reduced 45Ca2+ uptake is also manifest in adipocytes of septic rats. Alterations in adipocyte metabolism induced by ET include increased oxidation of glucose to CO2 (an insulin-like effect) and increased lipolysis upon NE and ACTH stimulation.
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PMID:Altered Ca2+ homeostasis and functional correlates in hepatocytes and adipocytes in endotoxemia and sepsis. 225 82

Altered glucose metabolism is one of the commonly observed sequelae of sepsis and septic shock. The present investigation was undertaken to determine the role of endotoxin (ET) upon hepatocyte glucoregulation, by measuring the activity of pyruvate kinase (PK), a key glycolytic enzyme. Hepatocytes were exposed to endotoxin concentrations known to occur in vivo during sepsis, i.e., from 1 X 10(-14) to 1 X 10(-8) g/ml. The alteration of the enzyme activities after addition of epinephrine, glucagon, insulin and calcium ionophore A23187 with and without ET preincubation were also examined. ET alone decreased the PK activity by 12% at all concentrations tested. The basal inhibition of the enzyme caused by epinephrine (-48%) was partially blocked by ET preincubation above 1 X 10(-10) g/ml. There were no ET-(glucagon, calcium ionophore, insulin) interaction. These in vitro results do not support pyruvate kinase as a site of hepatic enzyme regulation defect in endotoxaemia.
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PMID:Endotoxin, epinephrine, glucagon, insulin and calcium ionophore A23187 modulation of pyruvate kinase activity in cultured rat hepatocytes. 226 25


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