Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms responsible for renal insufficiency in septic shock (SS) have not been well characterized. We therefore investigated renal hemodynamics and the renal excretion of prostaglandin E2 (PGE2) in a nonhuman primate model of severe, low systemic vascular resistance (SVR) SS. In 18 cynomolgus monkeys, SS was induced by an infusion of 3 x 10(10) live Escherichia coli per kg; five saline-treated animals served as nonseptic controls. Systemic and renal hemodynamics, and urine PGE2 concentrations were determined over the 3 h after the induction of sepsis. The septic group demonstrated a significant (p less than .001) and sustained depression in both mean arterial pressure and SVR. Septic animals also had significantly lower effective renal plasma flow (ERPF) (p less than .01) and glomerular filtration rate (GFR) (p less than .01) compared to controls. Furthermore, the renal hemodynamic response to SS was biphasic, with significant increases in ERPF and GFR in the second hour postsepsis, followed by a pronounced decrease in the third postseptic hour. The septic group also demonstrated an increase in the renal excretion of PGE2 (p less than .001) that was temporally associated with the transient recovery in renal hemodynamics during the second postseptic hour. These sepsis-induced renal alterations may be important in the pathogenesis of renal insufficiency complicating clinical SS.
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PMID:Renal hemodynamics and prostaglandin E2 excretion in a nonhuman primate model of septic shock. 240 7

Among 140 patients with acute leukemia (AL) diagnosed according to FAB criteria, pericarditis was diagnosed clinically in 5 of them. They were 2 women and 3 men with different types of AL (L2-in one, M2-in one, M3-in one and M4-in two persons). It occurred in one patient at the onset of the disease and was associated with hyperuricemia, in another one--in complete remission, in the third--during partial remission, and in remaining two patients--during induction therapy. In all patients pericarditis was manifested by fever up to 38-40 degrees C, tachycardia and pericardial friction, in 3-heart silhouettes were enlarged. The ECG revealed mainly depression of ST segments. In 1 case only ECG pattern was typical of pericarditis. Clinically the symptoms of right ventricle failure predominated in 3 and of septic shock--in 2 patients. The etiologic factors were: Pseudomonas aeruginosa 2 X, Enterobacter cloacae 1 X, tuberculosis infection 1 X and hyperuricemia and Enterobacter sepsis 1 X. Pericarditis was favourably influenced by treatment with antibiotics, cardiaca and diuretics in 4 patients. One patient died of a sepsis. In no case the patient's death was attributable to pericarditis. The results of postmortem examinations in 79 cases of AL has revealed three additional cases of pericarditis due to tuberculosis infection, Staphylococcus aureus sepsis and aspergillosis.
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PMID:Pericarditis in the course of acute leukemia. 244 Jul 78

In the present study plasma fibronectin levels were determined in patients with hematopoietic malignancy, particularly leukemias, in an effort to clarify their clinical implications. Among leukemia patients, those with AML, ALL, ATL or CLL had various plasma fibronectin levels that were higher in some cases, while lower in others, as compared to normal control values. An elevation of the fibronectin level was noted often in APL, while lower fibronectin values were observed in many instances of CML. In these types of leukemia, acute exacerbation as well as supervention of infection tended to be associated with lower than normal levels of fibronectin. An especially marked depression of fibronectin occurred, when leukemia was complicated by sepsis or DIC, in which a good parallel was noted between the progress of disease and the fibronectin level. In lymphoproliferative diseases, the fibronectin value varied widely, but low fibronectin levels were frequently associated with intercurrent infection or an extreme deterioration of the general physical conditions.
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PMID:Variation of plasma fibronectin levels in leukemia patients. 248 45

The relationship between sepsis-induced CNS dysfunction and changes in brain blood flow remains unknown, and animal studies examining the influence of sepsis on cerebral blood flow (CBF) do not satisfactorily address that relationship. We measured CBF and cerebrovascular reactivity to CO2 in nine patients with sepsis syndrome using the 133Xe clearance technique. Mean CBF was 29.6 +/- 15.8 (SD) ml/100 g.min, significantly lower than the normal age-matched value in this laboratory of 44.9 +/- 6.2 ml/100 g.min (p less than .02). This depression did not correlate with changes in mean arterial pressure. Despite the reduction in CBF, the specific reactivity of the cerebral vasculature to changes in CO2 was normal, 1.3 +/- 0.9 ml/100 g.min/mm Hg. Brain blood flow is reduced in septic humans; the contribution of this reduction to the metabolic and functional changes observed in sepsis requires further study.
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PMID:Cerebral blood flow is reduced in patients with sepsis syndrome. 234 66

High surgical mortality in patients with obstructive jaundice and sepsis have been attributed to reticuloendothelial system (RES) depression. The purpose of this study was to clarify the effects of mechanical biliary obstruction on RES clearance of pathogenic bacteria by comparing the phagocytic index (K) with the directly measured hepatic uptake of indium 111-labeled bacteria injected into the portal vein of normal dogs and dogs with partial (PBO) or complete biliary obstruction (CBO). No significant difference was observed between the K in normal dogs (0.19 +/- 0.08; n = 6) and that in dogs with PBO (0.24 +/- 0.06; n = 5) or CBO (0.21 +/- 0.03; n = 4). There was no significant difference in uptake of radiolabel by the liver among the three groups of dogs. In our model, biliary obstruction had no effect on hepatic RES function and may not represent a significant determinant of mortality in patients with obstructive jaundice.
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PMID:Effects of biliary obstruction on hepatic clearance of bacteria. 250 73

Burn injury-induced changes at the neuromuscular junction include muscle weakness and altered response to neuromuscular blocking drugs. Protein malnutrition and sepsis can concomitantly occur with burn trauma. The role of pure malnutrition or sepsis, in the absence of burn injury, in inducing neuromuscular changes was studied in the mouse gastrocnemius muscle. Additionally, cAMP levels in muscle were evaluated to reflect metabolic activity. Sepsis was studied using doses of endotoxin at one-fourth or one-third the dose evoking 50% lethality. Diets of 5% protein and 5% protein + 35% fiber achieved protein and protein/calorie malnutrition, respectively. In each model neuromuscular function was evaluated by maximal tension developed. Pharmacologic responses were measured through effective dose to paralyze active tension by either 50 or 95%. Protein and protein/calorie malnutrition leading to an approximate 8% body weight loss caused a depression of maximal tension developed; this depression in tension was associated with a 10-fold increase in cAMP levels. Effective doses of d-tubocurarine for twitch inhibition during malnutrition were not significantly different from controls. Sepsis at 2 weeks caused an approximate 8% body weight loss, a significant decrease in maximal tension and at least a 3- to 5-fold shift to the right in dose-response curves to d-tubocurarine. In contrast to malnutrition, cAMP levels were significantly decreased (P less than .001) in sepsis to 1/400 of controls. The altered neuromuscular function and pharmacology observed in sepsis are similar to changes observed in burn injury. Protein malnutrition common to these two states may be important in functional but not pharmacological changes at the neuromuscular junction.
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PMID:Intraperitoneal endotoxin but not protein malnutrition shifts d-tubocurarine dose-response curves in mouse gastrocnemius muscle. 254 58

It is well known that patients who undergo surgical operations have a high risk of infection and sepsis. One explanation for this high risk may be a depression of neutrophil functions at the postoperative period. In the present study, the effects of surgical stresses on neutrophil functions were studied in ten patients who underwent general anesthesia and major surgery. The neutrophil functions especially focused on were the producing capacities of 5-lipoxygenase metabolites of arachidonic acid such as Leukotriene B4 (LTB4), LTC4, LTD4, 6-trans-LTB4, and w-oxidation products of LTB4. Neutrophils were stimulated with calcium-ionophore A23187 (2x10(-5) M) in the presence of arachidonic acid (5x10(-5) M) for 5 minutes at 37 degrees C. The arachidonic acid metabolites were extracted by methanol. After centrifugation, the supernatant of the mixture was concentrated and applied to a C-18 column on reversed phase high performance liquid chromatography (RP-HPLC) system, monitoring the absorbance at 280 nm. In all cases, the LTB4 production significantly increased postoperatively with an increment of 6-trans-LTB4 and w-oxidation products of LTB4. The LTC4 production, by contrast, significantly decreased postoperatively. LTD4 production was observed at neither pre nor postoperative periods. The total amount of LTA4 metabolites at the postoperative period, including LTB4, LTC4, and 6-trans-LTB4, increased 1.2 times compared with that at preoperative period. This indicates the possibility of the alteration of the neutrophil metabolism in 5-lipoxygenase cascade, the increment of LTA4 generation and the change of LTA4 metabolism from LTC4 synthesis to LTB4 generating pathway.
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PMID:Neutrophil producing capacity of 5-lipoxygenase metabolites of arachidonic acid after major surgery. 260 90

Neurological symptoms including lethargy, obtundation, and confusion are early and common findings in patients with sepsis. The etiology of the mental status changes that occur during severe infection is not known. We investigated the effects of sepsis on the levels of high-energy phosphates to determine whether decreased energy metabolism was a factor in the depressed neurological state. The time course of changes in brain pH and brain high-energy phosphate metabolites during an Escherichia coli infusion was determined from sequential phosphorus-31 nuclear magnetic resonance (31P-NMR) spectra of ketamine-xylazine-anesthetized rats. A second group of rats received 0.9% saline infusion and served as a control group. Despite severe obtundation and near loss of righting reflex, the rats in the septic group had no significant differences in the brain pH, the ratio of phosphocreatine (PCr) to beta-adenosine 5'-triphosphate (beta-ATP), or in the ratio of PCr to Pi. The only significant decrease in brain high-energy phosphates or pH occurred terminally in the septic rat group and corresponded with a rapidly falling arterial blood pressure. We conclude that the severe neurological depression that is characteristic of sepsis is not due to decreased levels of brain high-energy phosphates or brain acidosis.
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PMID:An in vivo examination of rat brain during sepsis with 31P-NMR spectroscopy. 261 Feb 45

Myocardial function in sepsis and endotoxin shock is reviewed. Clinical, whole animal, and isolated tissue studies are compared to answer the question whether sepsis and/or endotoxin directly damage the myocardium. Myocardial performance is considered relative to control of preload, afterload, and heart rate. Despite the fact that these vary widely in different studies, there is overwhelming evidence that myocardial performance is depressed in both sepsis and endotoxin shock. The depression is dose related, occurs early after large doses of endotoxin but may follow a hyperdynamic phase in sepsis or after low doses of endotoxin. Endotoxin itself does not appear to be the depressant factor; the final depressant substance(s) is unknown. Calcium transport by the sarcoplasmic reticulum is depressed. This defect is more prominent in the endocardium than in the epicardium. Myocardial adenosinetriphosphatase (ATPase) and norepinephrine stores may be depleted. The septic myocardium has an increased dependence on sympathetic nerve stimulation. There is little evidence that the cause of the myocardial depression is an inadequate coronary blood flow.
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PMID:Myocardial function in sepsis and endotoxin shock. 269 Jun 45

Severe sepsis leads to depression of the reticuloendothelial (RE) system with delayed bloodstream clearance of particulate matter and bacteria. Fibronectin may be an important opsonin of the RE system and low fibronectin levels often accompany severe sepsis in man. We have investigated the effect of prolonged intra-abdominal sepsis on plasma fibronectin concentrations and RE function. Serial plasma fibronectin concentrations were determined in rabbits for 2 weeks after either the induction of sepsis (appendix abscess) (n = 6) or laparotomy only (n = 6). RE function was measured at 2 weeks by determining the clearance kinetics and organ distribution of low dose technetium tin colloid (TTC). There was an early transient depression in plasma fibronectin values followed by elevated concentrations at 48-72 h which were more marked in the sepsis group. There was a delay in the blood clearance with reduced hepatic and increased bone uptake of TTC. We conclude that depletion of opsonic fibronectin is unlikely to be an important factor contributing to the impairment of RE function associated with intra-abdominal sepsis and that RE depression in septic animals is due to intrinsic Kupffer cell dysfunction.
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PMID:Reticuloendothelial failure in chronic intra-abdominal sepsis: the role of opsonic fibronectin. 270 51


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