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

Proline metabolism was prospectively evaluated in patients with surgical sepsis, cirrhosis, and elective surgical procedures. Significant correlations were found in the septic patients. Proline levels were an excellent indicator of mortality and correlated positively with lactate levels. Lactate and proline were inversely related to total peripheral resistance and oxygen consumption. In septic patients who expired: the metabolites involved in the hepatic pathways of proline degradation were elevated in proportion to proline; lactate, glutamate and proline were directly related to pyruvate; lactate/pyruvate ratios were constant; proline, glutamate, ammonia, ornithine, lactate and pyruvate levels were inversely proportional to oxygen consumption and total peripheral resistance. The primary defects in sepsis seem to be metabolic; there are very strong correlations in time between physiology and metabolism; the metabolic abnormality seems to be a progressive energy-fuel deficit, possibly from a progressive inhibition of substrate entry into the Krebs cycle.
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PMID:Proline metabolism in sepsis, cirrhosis and general surgery. The peripheral energy deficit. 11 5

Lactic acid is generated as the end product of anaerobic metabolism of glucose and is disposed by gluconeogenesis or oxidation. Changes in the lactate pyruvate ratio are not necessarily indicative of tissue hypoxia. The plasma lactate concentration is the result of lactate production and lactate removal (hepatic and renal gluconeogenesis; oxidation by muscle, liver and kidney). Lactic acidosis is defined as a state of metabolic acidosis (arterial pH less than 7.3) due to an increase in the blood concentration of lactate (greater than 2 mEq/l). Lactic acidosis may occur with evidence of tissue hypoxemia (type A) or in its absence (type B). Lactic acidosis has been described in association with phenformin therapy, hereditary enzymatic defects, hematological malignancy, prolonged fasting, shock with or without septicemia and occasionally without any underlying disease ("idiopathic" lactic acidosis). The therapy of lactic acidosis consists of administration of sodium bicarbonate and restoration of adequate tissue perfusion; hemodialysis may be helpful to control sodium excess and possibly to remove phenformin. The effectiveness of methylene blue, glucose and insulin are not yet established.
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PMID:Lactic acidosis. 87 61

The effect of ischemia on hepatic protein synthesis during sepsis is not known, but is of clinical relevance, since hepatic blood flow decreases during the late phase of sepsis. In this study, synthesis of acute-phase proteins was measured in perfused livers of rats 16 hours after sham operation or cecal ligation and puncture. Livers from each group had 45 minutes of complete ischemia or control perfusion. Protein synthesis was measured during two hour perfusion after the ischemia or control period, by determining incorporation of 3H-leucine into total secreted trichloracetic acid precipitated proteins, immunoprecipitated complement component C3 and albumin and phosphotungstenate-precipitated alpha 1-acid glycoprotein. Lactate, glutamine-oxalacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) levels in the perfusate were measured during preischemic and postischemic perfusion. Tissue glutathione levels were measured at the end of the perfusion. Synthesis of alpha 1-acid glycoprotein was increased by 100 per cent and albumin synthesis decreased by 46 per cent in septic livers, consistent with an acute-phase response and apparent downregulation of albumin synthesis during early sepsis. Synthesis rates were reduced by 50 to 60 per cent after ischemia in perfused livers from sham operated rats and 70 to 80 per cent in livers from septic rats. Hepatic production of interleukin-1 was not different between the groups during perfusion. GOT and GPT levels increased significantly during ischemia of both nonseptic and septic livers and rapidly returned toward baseline during reperfusion. Lactate levels were higher in perfusate of septic than of nonseptic livers before ischemia and increased further during ischemia. The results suggest that ischemia inhibits production of secreted hepatic proteins similarly in nonseptic and septic livers, but perhaps to a slightly greater extent in septic livers.
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PMID:Effect of ischemia on protein synthesis in the septic liver. 170 61

Pathologic oxygen supply dependency is an abnormal situation in which oxygen uptake (Vo2) varies directly with oxygen delivery. Its presence in patients with adult respiratory distress syndrome and/or sepsis has been associated with particularly high mortality rates that may be the result of tissue hypoxia that causes multiple organ failure. The evidence for this association has been indirect because we cannot use invasive methods that would be necessary to verify or disprove the hypothesis. Because further progress will depend on the development of adequate animal models of pathologic oxygen supply dependency, we have attempted to evaluate some of the available information in this area as well as the likelihood that tissue hypoxia will prove to be the precipitating factor. In anesthetized dogs injected or infused with endotoxin, many of the features of pathologic oxygen supply dependency have been successfully produced. These features include defective peripheral oxygen extraction, increased oxygen demand, and increased lactate levels. Regional measurements have shown that gut Vo2 decreases before other areas, particularly skeletal muscle. Lactate measurements alone were shown not to be sufficient proof of tissue hypoxia. More direct measurements of actual energy states and tissue Po2 are indicated for future research efforts.
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PMID:Experimental models of pathologic oxygen supply dependency. 202 22

Previously we studied levels of the cytokine IL-6 and activation of the complement and contact system and of neutrophils in a group of 48 patients with sepsis. Some of these inflammatory parameters appeared to be associated with a poor prognosis. Here we report on the relationships of C4a and C3a (complement activation products), of factor XII and prekallikrein (contact system proteins), of elastase (a protease released by activated neutrophils) and of the cytokine IL-6 to hemodynamic and biochemical parameters measured in those 48 patients at the time of admission to the Intensive Care Unit. No significant correlations between any inflammatory parameter and either systemic vascular resistance or cardiac index were found. Mean arterial pressure significantly correlated with both factor XII and prekallikrein levels. Lactate correlated with C3a and C4a, with elastase, and in particular, with IL-6, whereas it did not correlate with either factor XII or prekallikrein. Platelet numbers inversely correlated with both C3a and C4a, as well as with elastase and IL-6, whereas they positively correlated with factor XII and prekallikrein. Based on these findings we propose a model for the interplay of these inflammatory mediators in the pathogenesis of sepsis. This model takes into consideration the occurrence of capillary leakage, shock, disseminated intravascular coagulation, thrombocytopenia and of acute phase reactions in sepsis.
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PMID:A model for the interplay of inflammatory mediators in sepsis--a study in 48 patients. 228 88

The effect of sterile inflammation and sepsis on the release of lactate and amino acids by peripheral tissues was investigated in rats by removing the splanchnic organs (liver + small intestines) from the circulation and monitoring changes in blood metabolites over 30 min. Functional hepatectomy was performed in rats 5-7 days following the intraperitoneal introduction of a fecal-agar pellet (sterile vs. Bacteroides fragilis + E. coli). Lactate was significantly (P less than .05) increased in each of the conditions following hepatectomy but was raised to a significantly greater extent in sepsis (P less than .05). A similar response was observed for glutamine while alanine was only significantly (P less than .05) increased in sepsis following hepatectomy. Branched chain amino acids (BCAA) showed differential changes in sepsis compared to control. In control and sterile inflammation, functional hepatectomy was associated with significant decreases (P less than .05) in BCAA. In sepsis, BCAA were not decreased following hepatectomy and were significantly (P less than .05) elevated relative to control or sterile inflammation. Phenylalanine concentrations were not altered in control or sterile inflammation but were significantly elevated in sepsis (P less than .05). Insulin attenuated the accumulation of lactate and amino acids in fed control animals, following functional hepatectomy. However, in septic animals, insulin failed to prevent the rise in plasma lactate following hepatectomy.
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PMID:Role of extra-splanchnic organs in the metabolic response to sepsis: effect of insulin. 267 32

The severity of shock of 36 surgical ICU patients was classified using the Injury Severity Score (N = 20) and the Sepsis Score (N = 16). A great number of laboratory parameters were repeatedly determined on 5 days following the trauma or the onset of septic symptoms. Blood lactate, C-peptide, BUN, osmolality, and thyroid hormones were most closely related to the severity of the disease. This correlation was, however, less pronounced in the trauma than in the septic patients. Lactate and thyroid hormones showed a typical course in the non-survivors and may therefore be valuable as prognostic indices.
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PMID:Can the outcome after trauma or sepsis be predicted from biochemical or hormonal parameters? 311 1

Lactate concentrations in the cerebrospinal fluid of 104 patients were determined by the Monotest Lactate Kit. Lactate values were found higher in cases of bacterial meningitis than in patients not suffering from acute CNS disorders. Elevated lactate levels were also found in patients suffering from aseptic meningitis, septicemia, CNS trauma and cerebrovascular accidents, seizures and diabetes mellitus. The highest levels were found in cases of bacterial meningitis, but there was considerable overlapping between the groups. CSF lactate thus appears to have limited diagnostic value in the differential diagnosis between bacterial meningitis and other diseases with meningeal involvement.
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PMID:Value of CSF lactate in the differential diagnosis between bacterial meningitis and other diseases with meningeal involvement. 398 42

Lactate-buffered peritoneal solution traditionally has been used as dialysate for continuous renal replacement therapy (CRRT) in the United States because no bicarbonate solution is commercially available. Since 1994, the Cleveland Clinic Foundation Dialysis Unit has prepared a bicarbonate solution (sodium 144 +/- 3 mEq/L, HCO3 37 +/- 2 mEq/L, potassium 3 or 4 mEq/L, calcium 3.0 +/- 0.3 mEq/L, and magnesium 1.4 +/- 0.3 mg/dL) replicating the dialysate for chronic intermittent hemodialysis. No solute precipitation, as calcium or magnesium salts, were observed, and several cultures of the solution, performed at various time periods, remained negative. Fifty critically ill acute renal failure patients have been treated with bicarbonate-CRRT. All patients were in multiple organ failure and required mechanical ventilation; 37 were receiving vasopressors. Forty-four continuous venovenous hemodialysis sessions and eight continuous arteriovenous hemodialysis sessions were performed with a mean duration of 7.8 +/- 6.1 days. The mean inflow dialysate rate was 1,249 +/- 225 mL/hr and the mean outflow rate (dialysate plus ultrafiltration) was 1,399 +/- 237 mL/hr; the inflow rate was constantly kept lower or equal to the outflow rate to avoid an enhanced potential for backfiltration. No related fever spikes or sepsis episodes were noted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bicarbonate dialysate for continuous renal replacement therapy in intensive care unit patients with acute renal failure. 750 65

The liver oxygen delivery (DO2) and consumption (VO2) were measured in a porcine model of septic shock induced by fecal peritonitis. Lactate and hypoxanthine were simultaneously monitored in hepatic extracellular fluid and in central venous blood using a microdialysis technique. Animals were divided into a control group (n = 6) and a peritonitis group (n = 6). Peritonitis was induced by installation of a standardized amount of autologous feces into the abdominal cavity. The animals were followed for 5 h. The changes in the liver during peritonitis were, a decreased DO2, a increased, maintained, or decreased VO2, an increased oxygen extraction, and a loss of net hepatic lactate uptake. Parallel to these changes, systemic lactic acidosis developed. Intrahepatic lactate and hypoxanthine increased during peritonitis reflecting liver ischemia. The increase of these metabolites was seen concomitantly in the liver and in central venous blood. There was a wide variability of the individual response to the septic challenge among the animals. The limited hepatic oxygen delivery, and the increased needs for oxygen led to flow-dependent oxygen consumption, and signs of liver ischemia in severe sepsis. Intrahepatic and intravenous microdialysis may be useful for monitoring of the individual time course of hepatic and systemic ischemia in sepsis.
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PMID:Detection of liver ischemia using microdialysis during experimental peritonitis in pigs. 774 30


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