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

Cardiorespiratory and metabolic data were collected in 36 septic patients and 80 patients critically ill after nonseptic general surgery or trauma. Septic patients, particularly nonsurviving septics, showed early and sustained increases in metabolic rate, oxygen consumption, cardiac work, and minute ventilatory volume. They had lower levels of respiratory quotient and total peripheral resistance than nonseptic patients. High cardiac work was related to increasing oxygen transport. Both increases in metabolic utilization with high CO2 production, and abnormal increases in VD/VT appeared responsible for the higher minute ventilatory volumes. Respiratory quotient was negatively related to metabolic rate; this relation was modulated by the rate of caloric intake and, in nonseptic patients, was also influenced by the hemodynamic state. These data suggest that poor prognosis in sepsis is characterized by an early sustained stress response with more severe abnormalities in cardiovascular, metabolic, and respiratory function than is seen in the nonseptic stress response. The need for early support of physiologic functions and early and aggressive nutritional intervention is emphasized.
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PMID:Cardiorespiratory and metabolic adequacy and their relation to survival in sepsis. 641 5

Utilization of exogenous fat emulsion (Intralipid) in control, early septic, and late septic rats were studied. After intravenous infusion of 14C-Intralipid, cumulative amounts of 14CO2 in the expired breath in the 6-hr period were 42.8 +/- 1.8, 35.0 +/- 1.8, and 28.5 +/- 1.6% of the injected dose, respectively, for the three groups. The amount and the maximum rate of CO2 production correlated with the severity of sepsis. Significantly greater amounts of plasma triglyceride and free fatty acids were also observed in septic rats. The hyperlipemia associated with the observed decrease in plasma clearance of lipids may account for the decreased utilization of exogenous fat in septic rats.
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PMID:Utilization of exogenous fat emulsion (Intralipid) in septic rats. 642 68

Management of total parenteral nutrition (TPN) in depressed glucose metabolism was investigated clinically and experimentally in view of insulin control and/or new component of carbohydrate solution. Fifty TPN cases out of 837 for 9 years were successfully performed insulin control, while 17 patients were unable to get sufficient calory in spite of insulin administration. Cumulative expired CO2 after injection of radioactive carbohydrate in rats showed that each carbohydrate was utilized in the order of glucose, fructose, maltose, sorbitol and xylitol even in depressed glucose metabolism and that depressed carbohydrate metabolism was improved by adequate insulin injection. Combined use of glucose, fructose and xylitol at 4:2:1 (GFX) was was experimentally revealed to be superior to glucose alone as carbohydrate source of TPN in depressed glucose metabolism. Compared with conventional TPN (C-TPN), GFX-TPN showed lower blood glucose and insulin level in rabbits of sepsis and rats of streptozotocin diabetes. Contents of fructose 2,6 bisphosphate and triglyceride and activities of fructose 6 phosphate 2 kinase, acetyl CoA carboxylase and fatty acid synthetase in liver of these animals supported that GFX had favourable effects on glucose and fat utilization in depressed glucose Blood glucose of early postoperative patients was lower in GFX-TPN than in C-TPN.
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PMID:[Keypoints and compositions of total parenteral nutrition for patients with low glucose tolerance levels]. 643 89

Total parenteral nutrition (TPN) using glucose as nonprotein calories was associated with increases in O2 consumption (VO2) and CO2 production (VCO2). The magnitude of the changes was a function of the patient's clinical state and glucose load. Depleted patients showed a minimal increase in VO2, while VCO2 increased 23%. Minute ventilation (VE) increased 32%. Hypermetabolic patients (major trauma, sepsis) had a 30% increase in VO2 and a 57% increase in VCO2, while VE increased 71%. Patients with mild to moderate injuries (energy expenditure +/- 15% of normal) showed a 21% increase in VO2 and a 53% increase in VCO2, while VE increased 121%. Large carbohydrate intakes were associated with increases in CO2 production in all patients, while increases in O2 consumption were seen primarily in hypermetabolic patients. These changes suggest that the high glucose loads of TPN may be a physiologic stress.
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PMID:Respiratory changes induced by the large glucose loads of total parenteral nutrition. 676 43

The ventilatory response in acute lactic acidosis was assessed in 39 patients. In 18 patients, the acidosis was associated with phenformin ingestion and in 21, with other causes such as shock and sepsis, but not pulmonary edema. Arterial blood CO2 tensions and plasma bicarbonate concentrations were compared to those previously found in patients with uncomplicated diabetic ketoacidosis. In most of the lactic acidosis patients, arterial blood CO2 fell within the 95% confidence band calculated from the data in the ketoacidotic patients. Only 1 lactic acidotic patient had a triflingly lower CO2 tension. Shock was present in 8 of the 9 lactic acidotic patients whose CO2 tensions were more than 2 torr above the 95% confidence band.
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PMID:Ventilatory response in patients with acute lactic acidosis. 680 Jul 2

Previous investigations have demonstrated impairment of hepatic gluconeogenic activity during both hypovolemia and sepsis, but the mechanisms responsible remain unclear. The present study was designed to determine the influence of lack of oxygen on gluconeogenesis independent of humoral factors, products of ischemic peripheral tissues or pH changes. Livers obtained from Sprague-Dawley rats fasted 24 hours were perfused with Krebs-Henseleit buffer containing 5 mM lactate for 30 minutes. In the control group (n = 8) perfusion was continued; in others, anoxia was induced by perfusing with buffer equilibrated with 95% N2 and 5% CO2 for periods of 15, 30, or 60 minutes (n = 4, 5, and 5, respectively). The initial conditions were then reinstituted for an additional 45 minutes. Anoxia caused hepatic release of K+, indicative of disordered hepatic cellular ionic gradients and an abrupt cessation of gluconeogenesis. Reoxygenation partially reversed these alterations but some impairment of gluconeogenesis persisted and the degree of uptake of K+ from the perfusion media was decreased as the duration of anoxia increased. The degree of restoration of gluconeogenesis after a period of anoxia was closely associated with restoration of cellular uptake of K+. By comparison, livers taken from hypovolemic animals maintained at a mean arterial blood pressure of 40 mm Hg until the beginning of the decompensatory stage of shock exhibited a gluconeogenic capacity of only 41% of control animals and was comparable to the compromise induced by between 30 and 60 minutes of anoxia. These results suggest that the abilities to restore hepatic electrolyte balance and gluconeogenesis after oxygen deprivation are affected in parallel and may reflect a common dependence on the restoration of ATP stores after the insult.
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PMID:Effect of hemorrhage and anoxia on hepatic gluconeogenesis and potassium balance in the rat. 684 34

The course of the illness of a 56 year old female patient is reported, who is still surviving one and a half years after developing advanced, presumably progressive, so called "shock-lung syndrome". Following two episodes of hemorrhagic shock due to intestinal hemorrhage and post-operative secondary hemorrhage, interstitial lung edema developed, which was resistant to therapy. During the following weeks this was followed by bronchopneumonia with symptoms of sepsis persisting over several weeks. Between the third and seventh week of artificial ventilation X-ray of the lungs showed significant progressive changes of the interstitial tissues. This correlated with a progressive deterioration in gas exchange for O2 and CO2, which reached its peak in the seventh week with a paO2 of 71 mm Hg at a FIO2 = 1 and a paCO2 of 68 mm Hg at a minute volume of 15,51. The compliance of lung and thorax was severely reduced at 19 m1/cm H2O. At this apparently unfavourable time the patient was weaned off the respirator, and subsequently, over a period of three weeks, from oxygen insufflation. After eleven weeks of therapy, transfer to the medical ward was possible, with discharge from the hospital following three weeks later. The lung function tests at the time of discharge revealed a high grade reduction of all lung volumes and capacities without a significant obstructive component. The findings have shown a definite improvement during the following one and a half years. In retrospect the polypragmatic intensive therapy measures do not allow valid generalised therapeutic guidelines to be derived. We conclude, however, from this single observation, that therapeutic nihilism is not justified even in a progressive shock-lung syndrome which appears clinically and radiologically to be at an "irreversible" end stage.
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PMID:[Pulmonary fibrosis following ARDS. Case report of successful intensive therapy (author's transl)]. 711 41

Endotoxinaemia stimulates the generation of cysteinyl leukotrienes (LT), potent mediators of inflammation which are preferentially eliminated into the bile. Nitric oxide (NO) is a mediator molecule that has a possible protective role in liver injury. As sepsis and shock often lead to the development of hypoxic regions in the liver, the influence of hypoxia on the metabolism of cysteinyl leukotrienes and the hepatic production of NO were investigated in the isolated perfused rat liver. Livers were perfused in a non-recirculating haemoglobin-free system from the portal to the caval vein. Perfusion medium was equilibrated with 95% O2/5% CO2. In hypoxia experiments, gassing was changed to 95% N2/5% CO2 for 20 min. Tritiated leukotrienes were infused to the portal vein and metabolites in effluent and bile were measured by HPLC. Hypoxia did not influence the uptake of 3H-LTC4 and 3H-LTE4 but biliary elimination was reduced by 50-60% compared to normoxic control experiments. In hypoxia, the metabolite pattern in bile was also significantly changed with a decrease of omega-oxidation products. Following reoxygenation larger amounts of leukotrienes were excreted from the liver into the bile. To induce NO synthase in the liver, rats were injected intraperitoneally with endotoxin 6 hours before livers were isolated for perfusion. In contrast to nontreated livers, nitrite and nitrate, the oxidation products of NO, were detectable in the effluent perfusate. Basal NO2(-)+NO3- release was 5.3 (1.2) nmol/g liver/min. NO2(-)+NO3- release was stimulated by L-arginine infusion, whereas hypoxia resulted in an almost complete inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of hypoxia on nitric oxide formation and leukotriene metabolism in the perfused rat liver]. 751 4

The complex pathophysiology of adult respiratory distress syndrome (ARDS) makes preventive and therapeutic concepts difficult. Ample experimental evidence indicates that ARDS can be prevented by blocking systemic inflammatory agents. Clinically, only heparin, for inhibition of coagulation phenomena, is presently used among this array of approaches. Corticosteroids have not proven to be beneficial in ARDS. Alternative antiinflammatory agents are being proposed and are under current clinical investigation (e.g. indomethacin, acetylcysteine, alpha 1-proteinase inhibitor, antitumor necrosis factor, interleukin 1 receptor antagonist, platelet-activating factor antagonists). Symptomatic therapeutic strategies in early ARDS include selective pulmonary vasodilation (preferably by inhaled vasorelaxant agents) and optimal fluid balance. Transbronchial surfactant application, presently tested in pilot studies, may be available for ARDS patients in the near future and may have acute beneficial effects on gas exchange, pulmonary mechanics, and lung hemodynamics; its impact on survival cannot be predicted at the present time. Strong efforts should be taken to reduce secondary nosocomial pneumonia in ARDS patients and thus avoid the vicious circle of pneumonia, sepsis from lung infection, and perpetuation of multiple organ dysfunction syndrome. Optimal respirator therapy should be directed to ameliorate gas-exchange conditions acutely but at the same time should aim at minimizing potentially aggravating side effects of artificial ventilation (barotrauma, O2 toxicity). Several new techniques of mechanical ventilation and the concept of permissive hypercapnia address these aspects. Approaches with extracorporeal CO2 removal and oxygenation are being used in specialized centers.
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PMID:Prevention and therapy of the adult respiratory distress syndrome. 761 57

Earlier observations had indicated profound increases in the carbon dioxide tension of the myocardium, gastric wall, liver parenchyma, and renal cortex in the setting of extreme low-flow states of cardiac arrest and resuscitation, hemorrhagic shock, and anaphylactic shock. In venous blood draining the intestines, kidneys, and pelvic viscera, significant increases in PCO2 have also been observed during septic shock. In the present study, we investigated hepatic, renal, and cerebral cortical tissue carbon dioxide tension during intra-abdominal sepsis and shock in Sprague-Dawley rats. Peritonitis was induced by cecal ligation and fecal spillage. Over an interval of 320 +/- 60 minutes, we measured progressive reduction in mean aortic pressure from 152 +/- 11 mm Hg to 25 +/- 8 mm Hg and a decline in cardiac index from 492 +/- 75 ml/kg/min to 169 +/- 57 ml/kg/min. These hemodynamic deficits were accompanied by increases in liver tissue PCO2, from 58 +/- 4 mm Hg to 110 +/- 27 mm Hg (p = 0.006), in renal tissue PCO2, from 38 +/- 7 mm Hg to 115 +/- 24 mm Hg (p < 0.001), and in cerebral cortical tissue CO2, from 59 +/- 6 mm Hg to 108 +/- 16 mm Hg (p = 0.001). Arterial blood lactate content increased from 0.8 to 5.26 +/- 0.2 mmol/L (p = 0.001). Increases in blood lactate content preceded the changes in tissue PCO2 in each of these organs. These studies demonstrate that tissue hypercarbia is a more general phenomenon of low flow states, including that of circulatory shock associated with septic peritonitis.
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PMID:Hepatic, renal, and cerebral tissue hypercarbia during sepsis and shock in rats. 770


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