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

A guideline for early diagnosis of metabolic disorders affecting central nervous system during neonatal and early infancy was presented. Clinical manifestations associated with inborn errors of metabolism in the neonatal period are poor feeding, vomiting, diarrhea, abnormalities in muscle tonus, dyspnea, convulsion, coma and so on, and these are not specific to each disorder. However, such symptoms or signs as described below have often intimate relation to metabolic disorders: (1) previous children died of undetermined causes during early infancy; (2) complication of sepsis; (3) onset in the early neonatal period; (4) developmental and growth retardation. When newborns and infants have these symptoms or signs, we should start simple screening studies immediately for metabolic disorders, including CBC, hepatic function tests, blood glucose, lactate, pyruvate, ketone bodies, ammonia, blood gas analysis, urinalysis (including non-glucose reducing substance tests and FeCl3 reaction) and so on. As for CBC, we have to make our own effort to find spherocytosis and vacuoles in lymphocytes. Family history, especially the mother's personal history, is indispensable. During physical examinations, we must pay attention to facial appearance, skin color, macroglossia, hair abnormalities, peculiar odor of the urine and hepatosplenomegaly. When abnormality is found in these clinical signs or simple laboratory examinations, we should not hesitate to start dietary treatment even if special examinations for differential diagnosis are on the way.
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PMID:[CNS disorders caused by metabolic disorders]. 201 2

Two similar cohorts of low birth weight infants whose size was appropriate for gestational age randomly received either aztreonam-arginine plus ampicillin (n = 15) or gentamicin plus ampicillin (n = 15) for empiric treatment of neonatal sepsis. The regimens were infused together with glucose at greater than 5 mg/kg per minute, and immediate (4 hours) and cumulative (3 days) effects were assessed. Serum arginine and insulin values rose immediately after administration of aztreonam (containing 0.15 mmol of arginine per kilogram), but there were no changes in the gentamicin-treated cohort; no differences occurred in either cohort in serum concentrations of glucose, ammonia, potassium, creatinine, and bilirubin. After 3 days of antibiotic therapy (n = 13), the baseline serum arginine concentration was almost twice as high in the aztreonam group and showed a similar further rise and fall during the 4 hours after infusion; arginine urinary fractional excretion (normalized to creatinine clearance) decreased in the gentamicin group. The indirect bilirubin concentration rose more (p less than 0.001) in the aztreonam-treated infants (5.1 to 11.5 mg/dl (87 to 196 mumol/L] than in the gentamicin-treated infants (5.5 to 8.1 mg/dl (94 to 138 mumol/L)). Thus a modest differential bilirubin response and modestly elevated baseline serum arginine level occurred after the 3-day low-arginine doses of this study; serum ammonia and glucose concentrations were not affected. Aztreonam-arginine in neonates was well tolerated metabolically, and we believe that it can be used safely in conjunction with attention to glucose and bilirubin metabolism.
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PMID:Metabolic tolerance to arginine: implications for the safe use of arginine salt-aztreonam combination in the neonatal period. 204 Sep 35

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

A method for synthesis of zinc chlorophyllin a (I), a promising drug for clinical application, is presented. Taking silkworm faeces as a raw material. Chlorophyll was extracted with ethyl alcohol. After concentration the solid formed was dissolved in petroleum ether and the solution was subjected to column chromatography to separate pheophytin a and chlorophyll a. The products were dissolved in ethyl ether and the Mg in the products was stripped off with concentrated hydrochloric acid. The excess hydrochloric acid in the solution was neutralized with ammonia solution and the mixture was hydrolyzed with diluted hydrochloric acid to obtain pheophorbide a, then (I) was synthesized with pheophorbide a and zinc salt. The characteristics of (I) and pheophorbide a were checked by IR, UV and elemental analyses. All results of pheophorbide a coincided with those values reported in literature. The acute toxicity of (I) was tested in mice and the LD50 of (I) was 324 +/- 40 mg/kg. (I) has been applied in several hospitals for several months. It has been found that (I) has outstanding effects on burns and oral sepsis and that it increases the growth of granulation tissue and epithelium remarkably.
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PMID:[Synthesis of zinc chlorophyllin a and its preliminary clinical application]. 209 78

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

We elected to test the hypothesis that the metabolic encephalopathy associated with systemic sepsis may have a pathogenesis that is similar to hepatic encepathology, ie, as the consequence of hepatic dysfunction that induces alterations in synthesis of catecholic and noncatecholic neurotransmitters. Eleven patients with septic encephalopathy were compared with nine patients with septic encephalopathy and nine normal controls with respect to blood and cerebrospinal fluid (CSF) amino acid profile, phenylethylamine and its metabolite phenylacetic acid, and blood ammonia. Blood and CSF levels of phenylacetic acid increased markedly in septic and hepatic encephalopathy while CSF phenylethylamine levels were not increased in either condition, presumably due to rapid turnover. The CSF concentrations of all the aromatic amino acids were increased in hepatic encephalopathy, whereas in the patients with sepsis, only phenylalanine levels were increased. Evidence of stimulated neutral amino acid transport into brain was demonstrated in hepatic not septic encephalopathy and appeared to correlate with the CSF glutamine concentration. Blood ammonia levels were increased in hepatic but not in septic encephalopathy. Our data support the hypothesis that metabolites of phenylethylamine contribute to encephalopathy in systemic sepsis and hepatic failure; however, the entities differ in other respects.
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PMID:Septic encephalopathy. Evidence for altered phenylalanine metabolism and comparison with hepatic encephalopathy. 230 19

The intestinal metabolism of glucose and glutamine was studied in rats made septic by cecal ligation and puncture technique. Sepsis resulted in negative nitrogen balance and produced increases in the concentrations of blood pyruvate, lactate, alanine, and glutamine, and decreases in those of 3-hydroxybutyrate and acetoacetate. Both plasma insulin and glucagon concentrations were increased by 2.2- and 3.2-fold in septic rats, respectively. Portal-drained visceral blood flow increased in septic rats, and was accompanied by a decrease in the rates of utilization of glutamine and production of lactate, glutamate, and ammonia compared with those rates in sham-operated animals. Enterocytes isolated from septic rats showed decreased rates of glucose and glutamine utilization compared with cells isolated from corresponding controls. The maximal activities of hexokinase, 6-phosphofructokinase, pyruvate kinase, and glutaminase were decreased in intestinal mucosal scrapings of septic rats. It is concluded that a moderate form of sepsis decreases the rates of glucose and glutamine utilization (both in vivo and in vitro) by the epithelial cells of the small intestine. This may be caused by changes in the maximal activities of key enzymes in the pathways of glucose and glutamine metabolism in these cells as a metabolic adaptation to spare glucose and glutamine for use by other tissues.
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PMID:Glucose and glutamine metabolism in the small intestine of septic rats. 236 28

Immunoreactive plasma fibronectin depletion has been associated with the presence of collagen-fibronectin complexes in patients after trauma and in animal models of traumatic and burn injuries. However, the role of plasma fibronectin in the development of sepsis after traumatic and burn injuries in patients is unknown. Treatment of patients and animals with purified human plasma fibronectin ameliorates some of the clinical and metabolic effects of systemic endotoxemia. We report that the induction of immunoreactive plasma fibronectin deficiency by gelatin infusion is associated with enhanced effects of intraperitoneal Escherichia coli endotoxin injection. We have observed a significant increase in the concentrations of ammonia in plasma of treated rats compared with those in control rats administered the same dose of endotoxin.
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PMID:Enhanced endotoxin effects in plasma fibronectin-deficient rats. 329 66

In pigs subtotal ischemic liver cell necrosis was induced 4 days after auxiliary transplantation of 60% of the liver of an MLC-compatible donor (ATPL group, n = 13). In control animals (n = 14) temporary liver ischemia was preceded by division of the hepatic ligaments and creation of an end-to-side portacaval shunt. In the ATPL group six animals died of gastric hemorrhage, intestinal strangulation, or sepsis. The remaining seven animals survived in excellent condition until sacrifice 26 days after the induction of liver ischemia. Excellent graft function was demonstrated by uptake and excretion of 99mTc-HIDA at cholescintigraphy, ammonia detoxification, synthesis of clotting factors and glucohomeostasis. EEG recordings in the animals that underwent transplantation did not change from preischemic levels. Evidence of hepatic regeneration was found in the transplanted livers but could not be demonstrated in the damaged host livers. The control animals died in coma within 72 hours. These results indicate that auxiliary transplantation of a partial liver provides metabolic support and improves survival in animals with induced acute liver failure.
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PMID:Auxiliary transplantation of part of the liver improves survival and provides metabolic support in pigs with acute liver failure. 390 50

Several recent studies have suggested that solutions containing increased amounts of branched-chain amino acids (BCAA) might be useful in the treatment of patients with trauma and/or sepsis. In this study we investigated the optimal amount of BCAA in a balanced nutritional solution in an injured rat laparotomy model. The amino acid content of a standard BCAA-enriched amino acid solution was enriched to 40, 45, and 50% by the addition of equimolar amounts of the three BCAA. Rats were infused with either 3.6 cal/100 g body weight/24 hr or with 18 cal/100 g body weight/24 hr with either a 40, 45, or 50% BCAA mixture and evaluated for nitrogen balance, plasma amino acid levels, and levels of plasma blood urea nitrogen, creatinine, glucose, albumin, and blood ammonia. Nitrogen balance was negative in rats receiving only 3.6 cal/100 g body weight/24 hr, but was least negative in the group receiving 45% BCAA. Nitrogen balance was positive in groups receiving 18 cal/100 g body weight/24 hr, but was most positive in groups receiving 40 or 45% BCAA-containing solutions. Plasma amino acid patterns were least distorted in the 40 and 45% formulations. Blood ammonia was highest in the 40% BCAA group and plasma albumin was best maintained in the 45% BCAA group regardless of the amount of caloric supply. The results suggest that a 45% BCAA-enriched solution is the most appropriate in this injured rat model.
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PMID:The optimal branched-chain to total amino acid ratio in the injury-adapted amino acid formulation. 392 29


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