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

Fibronectin is a large-molecular-weight glycoprotein present on most cell surfaces, in extracellular fluids, and in plasma. Both cell-associated and soluble fibronectin are thought to have important roles in the inflammatory response and host defense and may contribute to the maintenance of microvascular integrity during septic episodes. Newborn infants have levels of fibronectin in plasma that are one-third to one-half those found in the healthy adult. In addition, neonates with respiratory distress syndrome, perinatal asphyxia, bacterial sepsis, intrauterine growth retardation, or postnatal malnutrition have a further depression in their plasma levels of fibronectin. The low plasma concentration of fibronectin in newborn infants may contribute to the hypofunction of the neonatal reticuloendothelial system and predispose to the development of sepsis. Rates of synthesis of plasma fibronectin are diminished in the neonate, and an inverse correlation between fibronectin half-life and gestational age exists. The role of fibronectin in treatment or prophylaxis of neonatal sepsis remains to be determined.
 ...
PMID:Role of fibronectin in diseases of newborn infants and children. 219 69

Septic shock is the commonest cause of death in intensive care units. Although sepsis usually produces a low systemic vascular resistance and elevated cardiac output, strong evidence (decreased ejection fraction and reduced response to fluid administration) suggests that the ventricular myocardium is depressed and the ventricle dilated. In survivors, these abnormalities are reversible. Failure to develop ventricular dilatation in nonsurvivors suggests that dilatation is a compensatory mechanism needed to maintain adequate cardiac output. With a canine model of septic shock that is very similar to human sepsis, myocardial depression was confirmed using load-independent measures of ventricular performance. Endotoxin administration to humans simulates the qualitative, cardiovascular abnormalities of sepsis. The pathogenesis of septic shock is extraordinarily complex. Diverse microorganisms can generate toxins, stimulating release of potent mediators that act on vasculature and myocardium. A circulating myocardial depressant substance has been closely associated with the myocardial depression of human septic shock. Therapy has emphasized early use of antibiotics, critical care monitoring, aggressive volume resuscitation, and, if shock continues, use of inotropic agents and vasopressors. Pharmacologic or immunologic antagonism of endotoxin or other mediators may prove to enhance survival in this highly lethal syndrome.
 ...
PMID:Septic shock in humans. Advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. 224 Sep 23

To further define cardiovascular abnormalities in patients with septic shock, serial conventional hemodynamic measurements combined with two-dimensional echocardiographic studies were performed at the bedside in 21 patients admitted for an acute episode of sepsis-related circulatory failure. Measurements obtained during the first hours of hospitalization revealed a group of six patients (group 1) with markedly depressed left ventricular function, as evidenced by a low cardiac index (CI) (2.2 +/- 0.8 L/min.m2), reduced left ventricular ejection fraction (LVEF) (21 +/- 8%), and an increased arterial-venous oxygen content difference. Right ventricular systolic function was also severely depressed. These patients were characterized as having sepsis-related cardiogenic shock secondary to profound myocardial depression, which was reversible within 24 to 48 h with inotropic support. The 15 remaining patients (group 2) exhibited an initially increased CI (4.9 +/- 1.8 L/min.m2), with a low systemic vascular resistance. In group 2, LVEF remained within the normal range despite abnormally low peripheral vascular resistance. This finding would suggest the presence of slight to moderate depression of left ventricular systolic function. All patients in this series had a normal left ventricular end-diastolic volume, whether profound myocardial depression was present or not.
 ...
PMID:Sepsis-related cardiogenic shock. 186 Mar 39

Late postinjury sepsis is largely the result of defective host defense including failure to maintain an adequate number of functioning phagocytic cells. In this study we used stem cell culture techniques to measure colony-stimulating activity and have quantitated the number of circulating myeloid stem cells to see if defects in granulopoiesis occur after major torso trauma. Forty-two acutely injured patients (13 blunt and 29 penetrating injuries; mean age, 29.7 years) undergoing laparotomy with an abdominal trauma index of 15 to 40 were studied prospectively. Blood samples were obtained on days 1, 5, and 10. Patients were segregated by injury severity: abdominal trauma index less than 25 (n = 25) versus abdominal trauma index greater than or equal to 25 (n = 17). The more severely injured (abdominal trauma index greater than or equal to 25) patients had fewer circulating granulocytes and monocytes. Colony-stimulating activity was below normal control levels in all patients and was decreased further with increased injury severity. The more severely injured patients had a blunted bone marrow response (significantly fewer circulating myeloid stem cells) and suffered more major septic complications (24% vs 8%). In conclusion, major trauma to the torso causes a paradoxic depression in granulopoiesis that worsens with increased injury severity and may contribute to late septic morbidity. This colony-stimulating activity deficiency state is similar to that seen after major burns and may be amenable to future modulation.
 ...
PMID:Inadequate granulopoiesis after major torso trauma: a hematopoietic regulatory paradox. 221 78

Although it is known that macrophage (M phi) functions such as phagocytosis and antigen presentation are depressed following hemorrhage and resuscitation, the mechanism remains unknown. The aim of this study was to determine, using scanning immunoelectron microscopic techniques, whether there is any alteration in the Fc receptors on the M phi after hemorrhage. To study this, male C3H/HeN mice were bled to a mean blood pressure (BP) of 35 mm Hg and maintained at that pressure for 1 hr, then resuscitated with their own blood and adequate fluids. Twenty-four hrs later, Kupffer cells from livers and splenic adherent cells were isolated, incubated for 16 hr, and then exposed to polysterene beads conjugated with antimouse IgG that specifically binds to Fc receptors. The cells were then prepared for observation by scanning electron microscopy. At least 100 cells from each animal were examined. The number of Kupffer cells from posthemorrhage mice that exhibited specific receptor labeling was significantly decreased (41.0 +/- 2.6, P less than 0.05) compared with control (64.2 +/- 7.5). The number of splenic adherent cells from posthemorrhage mice exhibiting specific receptor labeling was also significantly decreased (35.7 +/- 2.5, P less than 0.01) compared with control (61.2 +/- 3.9). The internalization of markers was also seen in some cells. The cause of the decrease in receptor labeling following hemorrhage may be the loss, inactivation, and/or internalization of receptors. Thus the decreased number of functional macrophages may contribute to the depression of antigen presentation and to the enhanced susceptibility to sepsis following hemorrhage.
 ...
PMID:Decreased Fc receptor expression on macrophages following simple hemorrhage as observed by scanning immunoelectron microscopy. 223 May 97

We investigated the effects of two different Gram-negative bacteria and radiation-induced leukopenia on endotoxemia, cardiovascular abnormalities, and mortality in a canine model of septic shock. Serial hemodynamics were measured in conscious dogs using radionuclide heart scans and thermodilution cardiac output catheters. Plasma endotoxin concentrations were determined with a chromogenic Limulus amebocyte lysate assay. Viable Pseudomonas aeruginosa or Escherichia coli implanted intraperitoneally produced concordant hemodynamic patterns of septic shock (p less than 0.01). Endotoxin concentrations were more than tenfold lower in dogs infected with P aeruginosa compared with E coli (p less than 0.0001). Despite lower endotoxin levels, P aeruginosa-infected dogs had a higher mortality (p less than 0.01), more severe hypotension (p less than 0.05), and greater depression of the left ventricular ejection fraction (p less than 0.05) than dogs with E coli sepsis. A nonlethal E coli challenge combined with leukopenia (induced by a nonlethal dose of radiation) resulted in a mortality of 60 percent (p less than 0.01) without greater cardiovascular dysfunction or higher endotoxin concentrations. These findings suggest that bacterial products other than endotoxin and host-related factors may be important contributors to the toxicity, cardiovascular instability, and mortality of Gram-negative septic shock. Quantitative determinations of plasma endotoxin are unlikely to correlate with the clinical severity of septicemia in heterogeneous patient populations infected with different Gram-negative organisms.
 ...
PMID:Pseudomonas aeruginosa compared with Escherichia coli produces less endotoxemia but more cardiovascular dysfunction and mortality in a canine model of septic shock. 224 91

Nutrition in acute spinal cord injury is complicated. Not every aspect of nutrition as it relates to the acutely injured spinal cord patient is known. The stress response to injury, fever, infection, sepsis, and surgery alter nutritional needs, as does the spinal cord injury itself. The sequelae of spinal cord injury, including denervation atrophy and paralysis, glucose intolerance, skin and wound breakdown, poikilothermy, anemia, respiratory paralysis, pneumonia, paralytic ileus, gastrointestinal ulcers and hemorrhage, neurogenic bowel and bladder, and depression, all affect the nutritional needs of the patient. Orthopedic appliances, pharmacologic agents, and other injuries can also alter nutritional requirements. Nutritional assessment in acute spinal cord injury is also complex. It should include medical and diet history, physical examination, intake and output measurements, prediction of energy expenditure and protein requirements, or--even better--measurements of energy expenditure with indirect methodology, using the metabolic cart or pulmonary artery catheter. Application of computerized tomography and radioisotope studies may prove valuable in the future. Finally, the direct relationship between nutrition and physiologic alterations of acute spinal cord injury necessitates that the critical care nurse incorporate nutrition-focused thinking into many aspects of the acute spinal cord--injured patient's care.
 ...
PMID:Nutrition in acute spinal cord injury. 226 60

There is evidence that undernutrition may contribute to the reduction in plasma fibronectin concentration and the depression of the reticuloendothelial (RE) system associated with severe sepsis. We have investigated the effects of fasting, surgical trauma and sepsis on plasma fibronectin concentrations and RE function. In experiment 1, plasma fibronectin was measured in rabbits (n = 14) before and 48 h after fasting. In experiment 2, sepsis was induced by devascularization of the appendix in animals on a normal diet (sepsis group, n = 7). A third group of animals underwent only a laparotomy (laparotomy only group, n = 7). Plasma fibronectin concentrations and the blood clearance and organ distribution of 99mtechnetium tin colloid (TTC) were measured 24 h after operation. Compared with pooled reference plasma, fasting in experiment 1 resulted in a reduction in mean(s.e.m.) plasma fibronectin concentration from 98(1.5) per cent to 86(3.7) per cent (T = 2, P less than 0.005). Mean(s.e.m.) plasma fibronectin concentration was raised in the sepsis group to 117(4.6) per cent, compared with 97(2.5) per cent in the laparotomy only group (U = 5, P less than 0.02), but there was no such increase in the fasting and sepsis group. There was a delay in the blood clearance and reduced hepatic uptake of TTC in both sepsis groups. The dissociation between fibronectin concentrations and RE function in animal models of sepsis casts doubt on the importance of fibronectin in RE function.
 ...
PMID:Effect of acute starvation on plasma fibronectin response to sepsis. 231 81

To identify cortical and subcortical structures in the brain which are associated with septic encephalopathy, local cerebral glucose utilization (LCGU) in the 31 discrete regions were evaluated with a quantitative (14C)-2.deoxyglucose autoradiographic method in the septic rat model. Sepsis was produced by cecal ligation and punctures. Forty rats were subjected to behavioral study and divided into two groups (control, n = 15; sepsis, n = 25). Septic rats died within 36 h, and the rats developed behavioral depression, and showed EEG slowing and an increase in pain threshold. The latter was evaluated by a tail flick method within 8 h after the surgical procedures, while control rats did not show significant change in either behaviors or pain threshold. In another study, LCGU was measured when behavioral depression, increase in pain threshold, and EEG slowing developed in the sepsis group (n = 7). In this group, the mean LCGU in auditory and parietal cortices, lateral geniculate, superior colliculus, hippocampus, and locus ceruleus was 95, 74, 67, 69, 72, and 53 mumol.100 g-1.min-1, being lower by 23%, 22%, 18%, 19%, 14%, and 27% than that in the sham-operated control group (n = 7), respectively. However, the mean LCGU in septal and raphe nuclei was 52 and 84 mumol.100 g-1.min-1, being significantly higher by 27% and 33% than that in the control group, respectively. These results suggest that septic encephalopathy is associated with metabolic changes in the discrete brain regions, which are related to the serotonergic or noradrenergic system.
 ...
PMID:Local cerebral glucose utilization in septic rats. 231 53

Previous studies describing the histologic elements of multi-system organ failure caused by bacterial sepsis may have been complicated by a significant interaction on tissue injury from either a preterminal low-flow state or the effects of therapy immediately before death. Therefore we evaluated the nonpulmonary histologic findings of sepsis during a 3-day period that followed cecal ligation and perforation. In this septic model, mean arterial perfusion pressures remained unchanged from baseline, systemic flows rose by 54%, and laboratory evidence of organ dysfunction including an elevation of the serum bilirubin levels and a depression of the serum total protein values was considered mild. Concurrently, development of the hyperdynamic central circulatory septic state was associated with widespread histologic changes in myocardium, striated muscle, liver, gut, and pancreas. Lesions common to these organs included high-protein interstitial and intracellular edema, mitochondrial destruction, and patchy cell necrosis. Lesions within the pancreas were exaggerated over those noted in other organs. Of all organs examined, only the liver demonstrated microvascular neutrophil accumulation. Unlike models of shock caused by sepsis, fibrin thrombi were not seen in the microvasculature of any organ. We conclude that tissue injury characterized by the accumulation of protein-rich extravascular fluid and the development of reversible and irreversible cell injury antedated significant multiple-system organ failure in this animal model of normotensive sepsis.
 ...
PMID:Histologic and ultrastructural changes in nonpulmonary organs during early hyperdynamic sepsis. 232 Nov 37


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>