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)

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

Immobilization-related hypercalcaemia is an uncommon but important condition being associated not infrequently with both urolithiasis and osteoporosis. In this study 5 patients who had been immobilized for a mean of 3 months and had a mean adjusted serum calcium of 3.15 mmol/l were treated with doses of intravenous pamidronate ranging between 10 mg and 45 mg. All patients became normocalcaemic by day 3. Patients 1-3 mobilized shortly after treatment and remained normocalcaemic. In those patients who continued to be immobile hypercalcaemia recurred after an interval of several weeks. Retreatment with pamidronate again resulted in normocalcaemia. No side effects were noted with treatment. All of the patients studied had increased rates of bone resorption as shown by elevated urinary hydroxyproline/creatinine ratios (median:range) of 0.101:0.045-0.180 (normal less than 0.033) and elevated calcium/creatinine ratios of 2.50:0.69-3.63 (normal less than 0.50). None of the patients in this study had any of the usual risk factors for developing immobilization-related hypercalcaemia though all 5 patients had problems with significant sepsis which we postulate may have lead to cytokine release which in turn contributed to the development of hypercalcaemia. We conclude that pamidronate (at doses as low as 10 mg) is safe and effective in immobilization-related hypercalcaemia and suggest that sepsis should be added to the list of risk factors for development of this syndrome.
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PMID:Immobilization-related hypercalcaemia--a possible novel mechanism and response to pamidronate. 226 2

From January 1976 through December 1988 we encountered ninety nine cases of intrahepatic stones. Eight of them were complicated with postoperative bile duct strictures which were formed on cholangiojejunostomy in 5 cases, cholangioduodenostomy, hepatic hilum and common hepatic duct in 1 case, respectively. Six cases of them are anastomotic strictures. The stones were mainly composed of bilirubin calcium. We guessed that the bile duct stricture resulted from cholangiojejunostomy without Roux-en-Y in 1 case and anastomotic insufficiency in 5 cases. Intrahepatic stones were removed by percutaneous transhepatic cholangioscopy (PTCS), and the treatment for the stricture was cholangiojejunostomy in 1 case and the dilatation by PTCS in 5 cases, including 3 endoprostheses by pig-tail silicone catheter and 2 internal-external biliary drainage. Two patients who did not undergo cholangioscopic dilatation died of sepsis due to cholangitis. Three of 5 patients who underwent endoscopic dilatation by PTCS could return to social life without recurrence of gallstones. In other two cases an endoprosthetic catheter was removed by PTCS because of dislodgement or obstruction of the catheter after confirming anastomotic strictures had improved. Authors recommended that PTCS should be applied for postoperative bile duct stricture complicated with intrahepatic stone.
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PMID:[A study on postoperative bile duct stricture with intrahepatic stones]. 227 19

Ionized Ca (Ca2+) is essential for maintaining physiologic functioning in the cardiovascular system (CVS). Sepsis affects the CVS by several mechanisms and is associated with decreased serum Ca2+. The pharmacodynamic response of the CVS to serum Ca2+ alteration was compared in acutely septic and nonseptic dogs at serum Ca2+ levels of 50%, 100%, 150% and 200% of normal baseline values. Serum Ca2+ alterations caused similar changes in both groups, although finite differences existed between septic and nonseptic subjects. Ca manipulation produced limited differences in the response of mean arterial pressure, cardiac output, left ventricular dP/dtmax, systemic (SVR) and pulmonary (PVR) vascular resistance between septic and nonseptic subjects. PVR and SVR demonstrated opposite responses during hypocalcemia; PVR was lower than baseline in both groups, whereas SVR was higher at the 50% level. No difference was evident for total oxygen consumption (VO2) or heart rate. In view of the limited differences in response and the failure to improve systemic VO2, serum Ca2+ supplementation does not afford any additional benefit in this experimental model of acute sepsis.
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PMID:Pharmacodynamic response to ionized calcium during acute sepsis. 237 5

Kupffer cell control of hepatocyte protein synthesis may be an important mechanism involved in the regulation of normal liver function and may be one mechanism responsible for the alterations in liver function seen during sepsis. The present series of in vitro experiments compare the response to various inflammatory stimuli of hepatocytes cocultured with Kupffer cells with that of hepatocytes cultured alone. In the absence of inflammatory stimuli, Kupffer cells stimulated hepatocyte protein synthesis. Lipopolysaccharide or gentamicin-killed Escherichia coli triggered Kupffer cell-mediated inhibition of cocultured hepatocyte protein synthesis but had no effect on protein synthesis of hepatocytes cultured alone. Phorbol myristate acetate, muramyl dipeptide, and calcium ionophore had no effect on hepatocytes cultured alone but resulted in a loss of Kupffer cell-mediated stimulation of cocultured hepatocyte protein synthesis without inhibition. Addition of dexamethasone to cocultures prevented the Kupffer cell-mediated inhibition of hepatocyte protein synthesis triggered by lipopolysaccharide, but did not block Kupffer cell-mediated stimulation in the absence of lipopolysaccharide. The data suggest that Kupffer cells can stimulate and inhibit hepatocyte protein synthesis by independent mechanisms. Kupffer cells may be important regulators of hepatocellular function in health and disease.
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PMID:Evidence that rat Kupffer cells stimulate and inhibit hepatocyte protein synthesis in vitro by different mechanisms. 249 43

Neutrophils can be "primed" for an enhanced respiratory burst by lipopolysaccharide (LPS) in concentrations measurable in patients with septic shock. Leukotriene B4 (LTB4) is the primary eicosanoid product of neutrophils and is felt to be a mediator of host defense and inflammation. We investigated the in vitro effects of LPS on neutrophil production of LTB4 and the omega-oxidation metabolites of LTB4. Incubation of neutrophils with LPS in concentrations ranging from 0.01 to 100 ng/ml did not result in production of LTB4 or metabolites in the absence of a second stimulus. Priming neutrophils with LPS and then stimulating with opsonized zymosan, phorbol-myristate-acetate or a low concentration of the calcium ionophore A23187 resulted in enhanced production of LTB4. LPS priming of neutrophils occurred in a concentration dependent manner. LPS did not result in LTB4 production in response to the chemoattractant peptide FMLP. LPS priming of neutrophils had no effect on cytosolic calcium concentrations of resting or zymosan-stimulated cells. These results suggest that LPS might effect host defense and tissue injury by potentiating the effect of other stimulants on neutrophil production of LTB4. This LPS induced enhancement may represent an important pathogenetic pathway in patients with gram negative sepsis.
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PMID:Bacterial lipopolysaccharides prime human neutrophils for enhanced production of leukotriene B4. 253 52


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