Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

The syndrome of symmetrical peripheral gangrene is characterised by distal ischaemic damage in two or more extremities, without large vessel obstruction. Four patients with bilateral pedal ischaemia are described and their haemodynamic profiles presented. In all four cases the syndrome developed in association with noradrenaline administration, sepsis and DIC, despite a high cardiac output and a low calculated systemic vascular resistance index. Early treatment with epoprostenol was instituted in the final case and was successful.
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PMID:Symmetrical peripheral gangrene: association with noradrenaline administration. 146 85

Immunological implications are important in every surgical operation, specially when it is necessary to remove the spleen. She plays an important role in immunological aspecific (filter, phagocytosis) and specific processes (production of IgM and regulation of T- and B-lymphocytic system). Splenectomy causes an immunodeficiency with frequent post-operative complications (the most important is OPSI). Each operated patient is considered generically immunodeficient because surgical trauma and anesthesiologic practice are at the base of immunological alterations (biological barriers, aspecific immunity, A.P.P., complement, specific immunity, NK cells). It's indispensable to know pathological situations that make "critical" the immunological state: caloric-proteic malnutrition, elderly (greater than 70 years old), immunosuppressive therapy, sepsis, shock, neoplasms. I. e.: a patient about seventy years old presents a reduced endocrine secretion of thymic hormone and, probably, a low synthesis of immunoglobulins. Besides the corticosteroids modify the answer of T-lymphocytes and NK cells. Sepsis induces metabolic and immunological alterations after early activation of humoral mediators, modified quantity and life of A.P.P., activation of complement, inhibition of cell-mediate immunity, modification of number and activity of haematic lymphocytes. Trauma induces a hypersecretion of corticosteroid, adrenalin, noradrenaline, glucagon with consequent hypercatabolism that causes malnutrition. The hormonal hypersecretion is a determining factor of reduced phagocytic activity (inhibited migration of neutrophils and monocytes), quantitative and qualitative alterations of complement, deficit of T-cells, hyporeactivity to skin test, depressed answer of antibodies to bacterial and viral antigens. Progressive neoplasms are characterized by modification of T-lymphocytes number, depressed macrophagic activity, hyporeactivity to skin tests.
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PMID:[Immunological implications of surgical intervention in critical and noncritical patients]. 175 43

This investigation compared the metabolic effects of lipid infusion in five septic and five nonseptic patients. Oxygen consumption was determined by indirect calorimetry over 1 h of rest and during 2 h when Intralipid (20%) was infused [166 mL/h; 23 kJ/min (5.5 kcal/min)]. Septic patients had a resting metabolic rate 17% higher than that of their nonseptic control subjects and a significant (P less than 0.05) rise (13%) in oxygen uptake was measured in both groups of subjects during the 2-h infusion of lipid. Preinfusion respiratory quotient (RQ) was 7% higher in the septic patients (P less than 0.05), and during the infusion period RQ decreased similarly (approximately 6%; P less than 0.05) in both groups. Plasma catecholamines were elevated in the septic patients preinfusion and the concentrations remained unaltered during the infusion. Norepinephrine rose significantly in the nonseptic group with the lipid infusion. The results show that sepsis has little or no influence on the characteristic rise in metabolic rate that occurs with intravenous lipid.
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PMID:Lipid infusion increases oxygen consumption similarly in septic and nonseptic patients. 198 40

The response of the sympathoadrenal system to hypoglycaemia of different etiology was studied in seven infants, aged 10-189 days. Five infants had hyperinsulinism secondary to nesidioblastosis or to a beta-cell adenoma of the pancreas, one infant had neonatal sepsis due to staphylococcal infection and one infant congenital growth hormone (HGH) and adrenocorticotropic hormone (ACTH) deficiency. In babies with hyperinsulinism, plasma noradrenaline increased from 0.29 +/- 0.03 to 0.61 +/- 0.09 ng/ml (P less than 0.01), whereas adrenaline increased only in three, but did not change in two babies. Increases in heart rate and blood pressure paralleled these changes. In hypoglycaemia due to congenital sepsis, noradrenaline increased from 0.39 to 1.64 ng/ml and adrenaline from 0.05 to 0.86 ng/ml. This was associated with marked haemodynamic changes. In congenital HGH and ACTH deficiency, the low basal plasma levels of noradrenaline (0.12 ng/ml) and adrenaline (0.01 ng/ml) remained unchanged in response to hypoglycaemia. Heart rate and blood pressure were unaffected. The sympathoadrenal system was activated by hypoglycaemia in all infants except in congenital HGH and ACTH deficiency. In contrast to adults, noradrenaline was the preferentially released catecholamine, suggesting an involvement of noradrenaline in glucose counter regulation in infancy.
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PMID:Sympatho-adrenal response to hypoglycaemia in infants. 285 Sep 15

Although nutritional support is vital to treatment of severe sepsis, the septic patient does not respond normally to glucose infusion. We have used the hyperglycemic glucose clamp technique to investigate the initial hormonal and metabolic responses of the septic patient to glucose under controlled conditions. The plasma glucose concentration was raised to and maintained at 12 mmol/liter for 2 hr in 12 septic patients and 11 normal controls. Glucose utilization, assessed from the amount infused, was significantly depressed in the patients, despite similar plasma insulin concentrations in the two groups. Forearm glucose uptake was similarly impaired. Despite very similar plasma free fatty acid concentrations in the two groups, which were suppressed equally by the glucose infusion, whole-body fat oxidation was elevated in the patients compared with the controls, and suppressed to a lesser extent in response to glucose. Glycerol and ketone body concentrations were elevated in the patients in keeping with a picture of accelerated release, clearance, and oxidation of fatty acids. Plasma cortisol, epinephrine, and norepinephrine concentrations were elevated in the septic patients in a severity-related manner, but not to high levels compared with experimental work. Norepinephrine showed no response to the glucose infusion in either group. Plasma glucagon concentrations were not significantly elevated in the septic patients. We conclude that the hyperglycemic glucose clamp provides a useful model for studying glucose intolerance in sepsis. Impaired glucose utilization in septic patients is associated with increased fat oxidation, although the hormonal basis for these changes is still unclear.
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PMID:Hormonal and metabolic responses to glucose infusion in sepsis studied by the hyperglycemic glucose clamp technique. 311 25

1. The effects of endotoxin (E. coli lipopolysaccharide, LPS) and heat inactivated group B Streptococcus (GBS) were studied on the contractile responses to noradrenaline (NA) in isolated pulmonary arteries and on the activity of the constitutive and inducible nitric oxide synthase (NOS) in lung fragments of neonatal piglets. 2. Short-term (< or = 5 h) incubation with LPS (1 micrograms ml-1) or GBS (3 x 10(7) colonies forming units ml-1) did not modify the vascular responsiveness to NA (10(-8) M-10(-4) M) in isolated intrapulmonary arteries. However, long-term incubation (20 h) with LPS or GBS produced a significant reduction in the maximal contractile responses and shifted the concentration-response curve for NA downwards. 3. Endothelium removal or the cyclo-oxygenase inhibitor meclofenamate (10(-5) M) did not affect the GBS- and LPS-induced hyporesponsiveness to NA. 4. The presence of the nitric oxide (NO) precursor, L-arginine (10(-5) M), 30 min prior to the contractility challenge increased the LPS- and GBS-induced pulmonary vascular hyporesponsiveness to NA. In contrast, the addition, prior to the challenge with NA, of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) or coincubation with dexamethasone (3 x 10(-6) M), a potent inhibitor of the induction of NOS, or with the protein synthesis inhibitor cycloheximide (10(-5) M) completely restored the reactivity to NA in LPS- and GBS-treated pulmonary arteries. 5. The incubation for 20 h of lung fragments with LPS and GBS produced a significant increase in the Ca2+-independent (inducible) NOS activity determined by the conversion of radiolabelled L-arginine to citrulline, but did not modify the constitutive NOS activity. This NOS induction was abolished by coincubation with dexamethasone (3 X 10-6 M).6. These results demonstrated that prolonged incubation with GBS and LPS causes an induction of NOS activity which results in a reduced vascular responsiveness to NA in pulmonary arteries of neonatal piglets. Thus, induction of NOS seems to be responsible for the delayed pulmonary vascular hyporesponsiveness induced by GBS (a Gram-positive) and E. coli (a Gram-negative), the most common causal agents of neonatal sepsis.
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PMID:Group B Streptococcus and E. coli LPS-induced NO-dependent hyporesponsiveness to noradrenaline in isolated intrapulmonary arteries of neonatal piglets. 754 18

Although depressed endothelium-dependent relaxation occurs during early sepsis, the precise mechanism responsible for this remains unknown. Because the elevated levels of plasma tumor necrosis factor (TNF) play a major role in the pathophysiology of sepsis, we investigated whether TNF-alpha administration alters endothelium-dependent relaxation. To study this, recombinant TNF-alpha (1.2 x 10(7) U/mg) was infused intravenously (0.25 mg/kg body wt) for 0.5 h in normal rats, and mean arterial pressure was monitored. At 1 h after the completion of TNF-alpha or vehicle infusion, the aorta and a pulmonary artery were isolated, cut into 2.5-mm rings, and placed in organ chambers. Norepinephrine (2 x 10(-7) M) was applied to achieve near-maximal contraction, and dose responses for an endothelium-dependent vasodilator, acetylcholine, and an endothelium-independent vasodilator, nitroglycerine, were determined. In additional studies, aortic rings from normal animals were incubated with TNF-alpha for 2 h in vitro, and vascular reactivity was determined. The results indicate that TNF-alpha administration significantly reduced acetylcholine-induced vascular relaxation both in vivo and in vitro. Such a reduction was sustained at least 80 min after the completion of 2-h incubation with TNF-alpha. In contrast, TNF did not alter nitroglycerine-induced vascular relaxation. Thus TNF-alpha depresses endothelium-dependent relaxation in vitro as well as in vivo. Because TNF-alpha infusion increases plasma TNF levels without decreasing mean arterial pressure, the depressed endothelium-dependent relaxation observed during early sepsis may be due to the elevated circulating levels of TNF.
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PMID:Administration of tumor necrosis factor-alpha in vivo depresses endothelium-dependent relaxation. 802 16

Sepsis and lipopolysaccharide (LPS) trigger the systemic release of both cytokines and catecholamines. Cytokines are known to be capable of eliciting a stress hormone response in vivo. The present study sought insight into the effect of noradrenaline on LPS-induced release of tumor necrosis factor alpha (TNF) and interleukin 6 (IL-6) in human whole blood. Whole blood was incubated with LPS for 4 h at 37 degrees C in the presence and absence of noradrenaline and/or specific alpha and beta antagonists and agonists. Noradrenaline caused a dose-dependent inhibition of LPS-induced TNF and IL-6 production. This effect could be completely prevented by addition of the specific beta 1, antagonist metoprolol, while it was not affected by the alpha antagonist phentolamine. Specific beta-adrenergic stimulation by isoprenaline mimicked the inhibiting effect of noradrenaline on LPS-evoked cytokine production, whereas alpha-adrenergic stimulation by phenylephrine had no effect. Fluorescence-activated cell sorter analysis demonstrated that beta-adrenergic stimulation had no effect on LPS binding to and internalization into mononuclear cells or on the expression of CD14, the major receptor for LPS on mononuclear cells. In acute sepsis, enhanced release of noradrenaline may be part of a negative feedback mechanism meant to inhibit ongoing TNF and IL-6 production.
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PMID:Noradrenaline inhibits lipopolysaccharide-induced tumor necrosis factor and interleukin 6 production in human whole blood. 816 70

Multiple organ failure is the major cause of death in patients with sepsis. Bacterial translocation from the gut is considered to induce and maintain sepsis. Therefore, the splanchnic region plays an important role in the pathogenesis and treatment of sepsis. There is evidence for a very high risk of imbalance between oxygen delivery and oxygen consumption especially in the splanchnic region. Consequently, there is a crucial interest whether it is possible to influence the splanchnic perfusion by specific catecholamines. Unfortunately, only a few, conflicting studies have looked at the effects of the various catecholamines on regional blood flow. Therefore, a clear recommendation for a specific catecholamine regimen in septic shock is impossible. Furthermore, it is unknown whether the choice of a specific catecholamine in the treatment of septic shock affects the patient's outcome. In most patients, the use of vasopressors is indispensable because adequate haemodynamic perfusion pressure is not achieved with fluid therapy alone. The negative effects of vasopressors on splanchnic perfusion are known from studies carried out under non septic conditions. Norepinephrine and dopamine in doses of 10 micrograms/kg/min in septic animals are without negative effects on splanchnic perfusion. Preliminary results show Preliminary results show a decrease in splanchnic oxygenation in patients with septic shock treated with epinephrine. Catecholamines with beta mimetic effects are often used to increase DO2. The question as to whether dobutamine or dopamine should be used first in treatment of septic shock cannot be answered yet. Whether treatment with low dose dopamine or dopexamine actually improves renal function and splanchnic oxygenation is the purpose of ongoing studies.
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PMID:Effects of catecholamines on regional perfusion and oxygenation in critically ill patients. 859 85


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