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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study elucidates the in vivo metabolic response of different liver cells after a single phagocytic challenge. In vivo glucose uptake of different tissues and isolated liver cells was determined by a sequential double labeling version of the 2-deoxyglucose technique. After latex administration, glucose uptake more than doubled in the liver, increased by about 50% in the spleen and lung and was not changed in muscle and testis. Within 10 min after intravenous injection of latex beads, neutropenia developed, with no change in the number of lymphocytes. This was accompanied by a marked influx of polymorphonuclear leukocytes into the liver. Latex was found in 52%, 35%, and 14% of the isolated Kupffer cells, polymorphonuclear leukocytes and endothelial cells, respectively. In vivo glucose uptake increased by 111%, 142%, and 43% in these cells. Glucose uptake by the latex-free hepatocytes was also elevated, presumably by way of intercellular signals between parenchymal and non-parenchymal liver cells. Indomethacin pretreatment resulted in the delay of neutrophil immigration into tissues without any change in the glucose response of different liver cells. Thus phagocytic stimulation in vivo results in marked neutropenia, migration of neutrophils into the liver, increased glucose uptake by phagocytic cells of the liver and enhanced glucose metabolism by the non-phagocytic parenchymal cells.
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PMID:Metabolic response of isolated liver cells to in vivo phagocytic challenge. 199 38

A rabbit model of group B Streptococcal (GBS) shock was used to study the effects of prostaglandin synthetase inhibition on the hemodynamic and hematologic response to GBS shock. The infusion of heat-killed GBS in groups I and II produced significant decreases in mean arterial pressure, neutrophil counts, and platelet counts (p less than 0.05), and significant rises in concentrations of thromboxane B2 and 6-Keto-PGF1 alpha, the stable metabolites of thromboxane A2 and prostacyclin (p less than 0.05). Administration of indomethacin (4 mg/kg) after GBS infusion (group II) was associated with a significant rise in mean arterial pressure and a significant decline in thromboxane B2 and 6-Keto-PGF1 alpha concentrations (p less than 0.05) but had no effect on GBS-induced hematologic alterations. Indomethacin administration before GBS infusion (group III) prevented alterations in mean arterial pressure and was associated with a decrease in thromboxane B2 and 6-Keto-PGF1 alpha concentrations. Indomethacin in group III did not prevent neutropenia and thrombocytopenia and may have exacerbated neutropenia. Alteration of experimental GBS shock with prostaglandin synthetase inhibition produces disparate hemodynamic and hematologic response.
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PMID:Prostaglandin synthetase inhibition in group B streptococcal shock: hematologic and hemodynamic effects. 309 76

Intravascular complement activation induces a rapid neutropenia and transient hypotension in laboratory animals such as rabbits. Injection of purified C5a causes similar hemodynamic events, and the hematologic changes suggest involvement of components such as polymorphonuclear leukocyte (PMN) and mediators including vasoamines and prostanoids. The anaphylatoxin-induced hypotension coincided with an increase in central venous pressure (CVP), decreased cardiac output (CO), increased plasma prostanoid levels, and neutropenia. These phenomena were repeatable in the animals when C5a was administered as a bolus 45 min after the initial treatment. Animals pretreated with indomethacin failed to exhibit the hypotensive response to C5a but still exhibited the transient neutropenia. Indomethacin effectively eliminated prostanoid release into plasma as expected. Administration of H2, but not H1, histamine-receptor antagonists reduced both C5a-induced hypotension and prostanoid release, suggesting that histamine may contribute to the C5a response in rabbits. Animals rendered neutropenic with nitrogen mustard prior to C5a challenge respond normally to C5a infusion (i.e., elevated prostanoid release and hypotension). The mechanism that we proposed for C5a-induced hypotension requires vascular smooth muscle contraction to be predominant over peripheral vasodilation in affecting cardiac output. Neutropenia occurs as a parallel event to hypotension but seemingly has little influence on the hemodynamic response. Prostacyclin (PGI2) levels were elevated in C5a-treated animals, and this lipid mediator contributes to hypotension by enhancing peripheral vasodilation. Because plasma TGxB2, levels were also elevated and central venous pressure increased as cardiac output decreased in treatment animals, we concluded that thromboxane-dependent pulmonary vasoconstriction contributes significantly to the C5a hypotensive response.
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PMID:Complement activation and membrane lipids in lung vascular injury. 361 9

A sheep model is described which produces acute pulmonary hypertension, leucopenia and hypoxia after blood, previously placed in contact with a Cuprophan hollow fibre artificial kidney, re-enters the circulation. Relationships between these manifestations (acute pulmonary hypertension, leucopenia and hypoxia) were examined in normal leucopenic and Indomethacin pre-treated sheep. The degree of pulmonary vascular response, and severity of leucopenia and hypoxia were all directly interrelated and were dependent upon the volume of blood injected. The induction of leucopenia did not affect the pulmonary hypertension or hypoxia. Pre-treating the animals with the cyclo-oxygenase inhibitor, Indomethacin, abolished both the pulmonary hypertension and the hypoxia without any effect on the development of neutropenia. These results suggest that leucocytes do not play a role in the haemodynamic response nor in the hypoxia; activation of the cyclo-oxygenase system is necessary for the development of acute pulmonary hypertension which causes hypoxia subsequent to alterations in ventilation perfusion relationships.
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PMID:Acute pulmonary hypertension, leucopenia and hypoxia in early haemodialysis. 399 92

Two patients with disseminated mycobacterial infection presented with severe neutropenia and hematopoietic failure. Marrow cells were obtained from each patient and were cultured in methylcellulose before and after the removal of mononuclear phagocytes, T-lymphocytes, or both from the marrow cell suspension. Glucocorticosteroid-resistant T-lymphocytes markedly inhibited granulopoiesis, but mononuclear phagocytes did not. Indomethacin inhibition of prostaglandin synthesis did not influence suppression of colony growth by the inhibitory lymphocytes. In the one patient who responded favorably to antituberculous therapy, the in-vitro T-lymphocyte inhibition of granulopoiesis disappeared as the neutropenia resolved. Thus, in some patients with disseminated mycobacterial infection, clinical bone marrow failure may be mediated, at least partly, by T-lymphocytes that suppress hematopoiesis.
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PMID:Suppression of granulopoiesis by T-lymphocytes in two patients with disseminated mycobacterial infection. 697 Oct 67

The role of eosinophils in granulopoiesis is unclear. In a variety of conditions, the level of eosinophils is inversely related to the level of neutrophils. The present report describes two patients with eosinophilia and neutropenia and examines the in vitro effects of eosinophils on the colony formation of their bone marrow in semisolid culture medium. The addition of autologous eosinophils to bone marrow cultures from these patients resulted in a decrease in the number of colonies; in contrast, antieosinophilic serum increased the number of colony-forming units. Indomethacin, an inhibitor of prostaglandin, was capable of reversing the effects of added eosinophils. The findings suggest that eosinophils have an inhibitory effect on in vitro granulopoiesis. The suppressive effects may be due to the high content of prostaglandin E found in eosinophils. A schematic diagram based on the current knowledge of the mechanism of granulopoiesis is presented.
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PMID:The role of eosinophils in granulopoiesis. I. Eosinophilia in neutropenic patients. 735 61

The effects of indomethacin, a cyclooxygenase inhibitor, upon plasma concentrations of prostaglandin E2 (PGE2), the febrile response, and metabolic and hematological alterations induced by lipopolysaccharide (LPS) were studied. Experimental endotoxemia was provoked via i.p. injection of 1.0 mg E coli LPS/kg in rats (group A). Indomethacin was introduced/os (2.5 mg/kg) 30 min prior to LPS challenge (group B). Pretreatment with this medication completely inhibited the hyperthermic response to LPS and eliminated the LPS-induced non-specific symptoms of anorexia, adipsia, reduced locomotory activity and gastrointestinal troubles. Plasma PGE2 concentrations increased as early as the 2nd h after the LPS challenge but were blocked when endotoxin application was preceded by indomethacin treatment. Indomethacin did not significantly influence hematological parameters. The dynamics of hematocrit and erythrocyte counts were similar in both groups with a decrease up to the 2nd h followed by an increase to maximum at post-treatment day 3. Pretreatment with indomethacin did not influence the endotoxin-induced leukopenia observed at the 2nd h or the accompanying neutropenia and left shift. Cyclooxygenase inhibition affected total protein concentrations; they were decreased in the early hours of the study (hours 4-6) in both groups. The later tendency towards increase in total protein concentrations was more expressed in animals from group B. Changes in blood glucose were characterized by a permanent tendency towards decrease after hour 2 of LPS challenge up to day 6 (group A). In group B, a similar tendency was observed, but glucose concentrations decreased between hours 2-6 and then returned to initial values.
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PMID:Effects of indomethacin on lipopolysaccharide-induced plasma PGE2 concentrations and clinical pathological disorders in experimental endotoxemia. 946 1