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

The activity of phosphate-dependent glutaminase and glutamine metabolism by tissues known markedly to utilize or synthesize glutamine (or both) were studied in rats made septic by cecal ligation and puncture technique and compared with the same measures in rats that underwent sham operation (laparotomy). Blood glucose level was not markedly different in septic rats, but lactate, pyruvate, alanine, and glutamine levels were markedly increased. Conversely, blood ketone body concentrations were significantly decreased in septic rats. Both plasma insulin and glucagon levels were markedly elevated in response to sepsis. The maximal activity of phosphate-dependent glutaminase was decreased in the small intestine, increased in the kidney and mesenteric lymph nodes, and unchanged in the liver of septic rats. Arteriovenous concentration difference measurements across the gut showed a decrease in the net glutamine removed from the circulation in septic rats. Arteriovenous concentration difference measurements for glutamine showed that both renal uptake and skeletal muscle release of the amino acid were increased in response to sepsis, whereas measurements across the hepatic bed showed a net uptake of glutamine in septic rats. Enterocytes isolated from septic rats exhibited a decreased rate of utilization of glutamine and production of glutamate, alanine, and ammonia, whereas lymphocytes isolated from septic rats showed an enhanced rate of utilization of glutamine and production of glutamate, aspartate, and ammonia. It is concluded that, during sepsis, glutamine uptake and metabolism are enhanced in renal and lymphoid tissue but decreased in that of the small intestine, with increased rates of release by skeletal muscle; however, the liver appears to utilize glutamine in septic rats.
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PMID:Maximal activity of phosphate-dependent glutaminase and glutamine metabolism in septic rats. 206 39

The pathogenesis of sepsis in acute pancreatitis is unknown. Since the intestinal tract has recently been identified as a possible source for sepsis in other conditions, we explored whether the gut may serve as a reservoir for bacteria causing systemic and pancreatic infection in acute pancreatitis. Bacterial translocation, alterations of intestinal microflora, and intestinal motility, as reflected by gut propulsion, were studied in a rat pancreatitis model. Acute pancreatitis was induced by biliopancreatic obstruction (AP); sham manipulated animals served as controls (sham). Bacteriologic cultures were obtained from various segments of the intestinal tract and from blood, liver, spleen, pancreas, and mesenteric lymph nodes 48 and 96 hr after induction of AP or sham. Bacteria were recovered from mesenteric lymph nodes of all 12 animals with AP, but only from 3/14 sham animals (P less than 0.05). Spread to distant organ sites occurred in 4 of 12 animals with AP compared to none of the sham animals (P less than 0.05). A disruption of the intestinal microflora was found in the cecum, where the gram-negative bacterial count (log/g) was significantly higher during AP when compared with sham controls: 10.62 +/- 1.04 vs 8.05 +/- 1.45 at 48 hr and 7.92 +/- 0.62 vs 6.79 +/- 0.87 at 96 hr, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of the gut in the development of sepsis in acute pancreatitis. 206 54

Transient episodes of gut mucosal ischemia occur in many patients having cardiac surgery. Ischemic mucosal injury increases mucosal permeability and promotes the translocation of bacterial toxins and bacteria and, hence, the release of mediators. Collectively these substances are the putative cause of LOS, nosocomial infections, and MSOF. Circumstantial evidence suggests that the morbidity and mortality from cardiac surgery might be greatly reduced by preventing or limiting in duration the episodes of gut mucosal ischemia. This objective is unlikely to be reliably achieved in clinical practice without monitoring the adequacy of gut mucosal oxygenation. The adequacy of gut mucosal oxygenation can be conveniently monitored in the stomach with a Tonomitor incorporated into a nasogastric tube, because changes induced in this organ by disturbances in DO2 reflect changes occurring in other parts of the gut. Preventative measures currently possible in routine clinical practice include maintaining an intramucosal pH at normal levels by optimizing DO2, preventing the release of splanchnic vasoconstrictors and the formation of cellular aggregates by the use of pulsatile perfusion during bypass, and minimizing oxygen requirements with cooling and muscle relaxation. The translocation of bacterial toxins and bacteria across injured mucosa may be minimized by gut lavage before surgery. Therapeutic measures for gut mucosal ischemia currently possible in routine clinical practice include, in addition to the preventative measures outlined above, the prevention of free radical-induced mucosal injury during resuscitation, parenteral antibiotics, the treatment of sepsis, and the resection of infarcted gut.
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PMID:Gut mucosal ischemia during cardiac surgery. 209 99

Nutritional support of critically ill patients is important since adverse effects of malnutrition are multiple and common. Nutrition via the enteral route is often preferred over central venous or total parenteral nutrition due to its relative ease of administration, lower cost, and infrequent association with severe complication. Enteral nutrition and infection are related. Infectious complications of sepsis and nosocomial pneumonia can occur, but enteral nutrition also may be important in maintenance of normal gut structure and function, thereby decreasing bacterial translocation and the risk of systemic infection.
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PMID:Enteral nutrition and infection in the intensive care unit. 212 89

Infections due to Gram-positive bacteria, especially coagulase-negative staphylococci, have been increasing in immunocompromised patients during the last 5 years because of an increased use of Hickman catheters and oral gut decontamination with quinolones. Teicoplanin, a new glycopeptide antibiotic, has a long plasma half-life which allows once-a-day bolus administration, making it a 'user friendly' agent. A randomized comparative evaluation of teicoplanin plus aztreonam versus gentamicin plus piperacillin in leukaemic patients with a clinical diagnosis of septicaemia was undertaken. The objectives of this study were (1) to evaluate the efficacy and safety of teicoplanin and aztreonam in comparison to a 'standard antibiotic' regimen and (2) to assess the local and systemic tolerance of these drugs. Results of the study in more than 70 patients to date are presented, and the role of anti-Gram-positive antibiotics in the management of severe sepsis in immunocompromised patients is discussed.
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PMID:A comparative efficacy and safety study of teicoplanin plus aztreonam versus gentamicin plus piperacillin in haematology oncology patients with clinically diagnosed septicaemia. 214 49

Gram-negative infections in neutropenic patients originate frequently from the gut flora. Attempts to decrease the incidence of these infections have utilized several regimens for gastrointestinal decontamination, of which some have proven to be clinically useful. Orally administered nonabsorbable antibiotics (aminoglycosides, polymyxins) can decrease the incidence of gram-negative sepsis during neutropenia, but, with the possible exception of netilmicin, tolerance to these agents is generally poor, and compliance is low. Trimethoprim-sulfamethoxazole has been used widely for the prophylaxis of infections in neutropenic patients. Clinical results with this agent have been conflicting, as its efficacy is clearly related to epidemiological patterns of resistance of the pathogens in the population under study. More recently, the quinolones, which are well tolerated by patients and are presently active on most strains of Enterobacteriaceae, have been associated with a virtual eradication of gram-negative infections in neutropenic patients. These results have been paralleled by an increase in the frequency of gram-positive infections, which, fortunately, cause an incidence of mortality that is much lower than that seen in gram-negative sepsis. The fact that the quinolones are absorbed systemically might help to explain their efficacy in chemoprophylaxis during neutropenia. This paper discusses the chemoprophylaxis of gram-negative infection during neutropenia in the light of theoretical concepts such as 'colonization resistance', 'selective decontamination', and 'bacterial translocation'.
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PMID:Chemoprophylaxis of gram-negative infections in neutropenic patients. 216 99

Since its first description in 1967, the mortality of the adult respiratory distress syndrome (ARDS) has remained unchanged despite the increasing sophistication of supportive techniques. Few patients now die of refractory hypoxemia, the majority succumbing to the multiple systems organ failure syndrome, commonly due to sepsis. Sepsis is both the most common cause of ARDS, usually involving the abdomen, and the most frequent complication, usually affecting the lungs. ARDS is, thus, increasingly seen as the pulmonary component of multiple systems organ failure, triggered by the systemic response to sepsis. In critically ill patients, impairment of hepatic function and of the barrier function of the gut mucosa allows translocation of endotoxin derived from the aerobic Gram-negative bacteria within the gut. This releases mediators which are responsible for the activation of cellular and humoral cascades, resulting in the pathological changes seen in ARDS. This sequence of events underlines the importance of therapies directed at abnormal colonization of the gastrointestinal tract and elimination of the gut endotoxin pool. Selective decontamination of the digestive tract is attractive in that it attacks the problem from 2 sides: first, by eliminating colonization, it appears effective in preventing secondary infection and, second, it may also play a role in reducing the enteric endotoxin pool. Recent descriptions of pathological oxygen supply dependency in both ARDS and septic patients emphasize the similarity of pathophysiological abnormalities in the 2 conditions. Intensive supportive therapy to achieve adequate oxygen transport and aggressive investigation and surgical management of septic foci are the cornerstones of management of the established syndrome.
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PMID:Intraabdominal infection: pulmonary failure. 218 82

In the critically ill surgical patient a variety of therapeutic maneuvers is required to maintain a "healthy gut." Provision of adequate amounts of glutamine to the gastrointestinal mucosa appears to be just one of these maneuvers. Other methods utilized to protect the gut from becoming a wound include: (a) minimizing additional systemic insults (such as hypotension, sepsis, multiple operative procedures); (b) aggressive pulmonary care; (c) the judicious use of antibiotics; and (d) aggressive enteral or parenteral feedings. The concept that the gut is an organ of quiescence following surgical stress merits reconsideration. The intestinal tract plays a central role in interorgan glutamine metabolism and is a key regulator of nitrogen handling following surgical stress. Critically ill patients are susceptible to developing gut-origin sepsis, the incidence of which will be diminished by instituting measures and providing treatments which support intestinal structure, function, and metabolism. Provision of glutamine-enriched diets to such patients may be one of these therapies.
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PMID:The role of glutamine in maintaining a healthy gut and supporting the metabolic response to injury and infection. 218 15

There is accumulating evidence that multiple organ failure is not always the result of an established septic focus. Increasing attention has centred on the gut as a reservoir of bacteria (and bacterial endotoxins) that can traverse the intestinal mucosal barrier (a process called 'bacterial translocation') and initiate the septic state. Although the link between haemorrhagic shock and sepsis was recognized decades ago, the full experimental demonstration of this phenomenon is more recent. It was shown to occur in three main settings: physical disruption of the gut mucosa, impaired defence mechanisms and altered gut microbial ecology. Conditions such as haemorrhagic shock, burns, protein malnutrition and sepsis are seen in the severely ill surgical patient or the multiply injured, and are known to cause various combinations of circumstances favourable to bacterial translocation and endotoxin absorption. These may play an important role in the mortality of the critically ill.
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PMID:Gut barrier function and the surgeon. 219 47

Tumor necrosis factor (TNF), a polypeptide produced predominantly by activated macrophages, is an important mediator of sepsis. We analyzed the specific metabolic changes that occur in the gut following TNF administration. Following general anesthesia, hemodynamic and metabolic indices were measured serially in control dogs (n = 7) and animals receiving a continuous sublethal intravenous infusion of TNF (0.57.10(5) IU/kg/6 hours, n = 7). During TNF infusion mean arterial pressure gradually decreased despite fluid administration, which maintained wedge pressure and cardiac index, which were similar to control animals. While TNF significantly reduced intestinal blood flow to 12 +/- 3 mL/min/kg compared to 28 +/- 3 mL/min/kg (p less than 0.01) in controls, intestinal oxygen consumption was maintained due to an increased extraction rate. Despite hypoperfusion the intestinal exchange of metabolic substrate (glucose, lactate, pyruvate, alanine, glutamine, glutamate, and ammonia) was comparable between the control and TNF-infused animals. However, when substrate carbon balance across the intestinal tract was calculated, it appeared that there was a limitation in fuel availability in the TNF animals. This may be due to competition for fuel between the gut and other major organs. Fuel limitation may jeopardize rapid cell proliferation and mucosal repair and with regional hypoperfusion these processes may account for the mucosal ulcerations observed at the termination of the study.
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PMID:The effects of tumor necrosis factor on intestinal structure and metabolism. 225 57


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