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PubMedDate not supplied

Modification of galactosamine-induced liver injury in rats by reticuloendothelial system stimulation or depression.

The reticuloendothelial system has been implicated in galactosamine-induced liver injury because of a correlation between phagocytic alterations induced by colloidal carbon or endotoxin, and development of liver necrosis. To evaluate this concept, the influence of galactosamine on liver function and histology was determined in rats in which the reticuloendothelial system was normal, stimulated, or depressed. Methyl palmitate was used as a reticuloendothelial system suppressant, and glucan was used as a reticuloendothelial system activating agent. Administration of galactosamine to control rats resulted in hypoglycemia and increased serum bilirubin concentration, elevated serum glutamic oxalacetic transaminase, lactic dehydrogenase and glutamic pyruvic transaminase activities, and retention of sodium sulfobromophthalein. Histological studies revealed hepatic necrosis, and a polymorphonuclear and lymphocytic cellular infiltrate in galactosamine-treated rats. Pretreatment of rats with methyl palmitate inhibited galactosamine-induced alterations in serum glucose concentration, glutamic oxalacetic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammatory reactions were also reduced in methyl palmitate-treated galactosamine-injected animals. In contrast, activation of the reticuloendothelial system by glucan increased galactosamine-induced alterations in serum bilirubin, glucose and cholesterol concentrations, glutamic oxalacetic transaminase, glutamic pyruvic transaminase and lactic dehydrogenase activities, and sodium sulfobromophthalein retention. Liver necrosis and inflammation were also increased. These findings suggest that the degree of galactosamine-induced liver injury is directly correlated with macrophage function when specific macrophage-modifying agents are used.

Animals↗
PubMed2000

Hyperthermic effects on reticuloendothelial system particulate uptake.

Reticuloendothelial system (RES) particulate uptake (PU) of vascular debris influences survival from extreme hyperthermia. Little is known of the effect of extreme hyperthermia, unrelated to fever, on RES PU shortly after reaching a maximum core temperature (T(c)). Relative to normothermic rats (T(c)=38.0 degrees C), rats at T(c)=42.6 degrees C had significantly higher, while T(c)=42.0 degrees C rats had significantly lower total RES tissue (lung, liver, spleen) PU of fluorescent microspheres (1 µ), when compared to rats at T(c)=42.6 or 38.0 degrees C. These findings suggest at T(c)=42.6 degrees C, rats were not actively thermoregulating. As such, more blood remained in the core than in the periphery, which resulted in greater core RES tissue PU. In contrast, to reduce or control core heat, rats at T(c)=42.0 degrees or 38.0 degrees C directed more blood to the periphery, which reduced core RES tissue PU. Blood flow patterns as directed by the state or degree of active thermoregulation is likely an influence of hyperthermia on RES PU.

Journal Article↗
PubMedDate not supplied

Reticuloendothelial system Fc receptor function in systemic lupus erythematosus.

Reticuloendothelial system Fc receptor function was measured in 10 patients with systemic lupus erythematosus (SLE) taking corticosteroids, 10 SLE patients not receiving corticosteroids and in 19 controls, 9 of whom were corticosteroid-dependent asthmatics and 10 of whom were healthy. Clearance studies were performed using autologous 51 Cr-labeled erythrocytes that had been sensitized with human IgG anti-Rh(D) [6,700 molecules/cell]. The clearance curves could be split into a fast (t1/2 fast) and a slow (t1/2 slow for any of the groups of patients. The results were correlated with serum C3, C4, DNA-binding, fluid phase 125I-Clq binding, a disease activity index, corticosteroid dose and duration of therapy with corticosteroids. The only significant correlation was an inverse correlation of C4 with the t1/2 slow in SLE patients not on corticosteroids (r=- 0.71, p less than 0.05). The t1/2 slow of the 3 SLE patients with active nephritis (86 +/- 40 min) was significantly different from the 17 SLE patients with inactive nephritis or normal renal function (37 +/- 5 min) (P less than 0.05). We conclude that there is no overall defect of Fc receptor function in our patients with SLE although there is decreased clearance in patients with active lupus nephritis.

Asthma↗
PubMed1980

[Physiology and pathophysiology of the reticuloendothelial system of the liver (author's transl)].

The reticuloendothelial system of the liver includes endothelial cells, Kupffer cells, fat storing cells and pit cells. Kupffer cells have special surface structures, the so-called fuzzy coat and immunological receptors, which are responsible for phagocytotic activity. The physiological role of the hepatic reticuloendothelial system is clearing various substrates as for instance proteins and lipoproteins, hemoglobin, bilirubin, immune complexes, bacterial toxins, and certain circulating cells. The activity of the reticuloendothelial system can be influenced by blood flow velocity, by opsonins produced by the body itself, and by certain exogenous factors. The function of the reticuloendothelial system may be estimated by methods, which are dependent essentially upon hepatic clearance of intravenously applied, special substances.

Animals↗
PubMed1981

Modification of glomerular immune complex deposition in mice by activation of the reticuloendothelial system.

To determine the effect of activation of the reticuloendothelial system on the localization of immune complexes in the kidney, a model of passive serum sickness nephritis in the mouse was used, with activation of the reticuloendothelial system with Corynebacterium parvum. Groups of mice, control and C. parvum-treated animals, were injected with BSA-125I-anti-BSA complexes containing 3 mg 125I-anti-BSA. Blood was obtained at 5 min, at 3 h, and at 12 h, when the animals were killed. Blood concentrations of BSA-125I-anti-BSA complexes were reduced in C. parvum-treated animals compared with controls. This appeared to be mediated by two effects, increased uptake of complexes in the liver and spleen, and enhanced degradation of immune complexes as measured by TCA-soluble radioactivity. In vitro studies using cultures of peritoneal macrophages also showed enhanced uptake of immune complexes. The amount of immune complexes deposited in the glomeruli of C. parvum-treated animals was reduced as determined by quantitation of radiolabeled material bound to isolated gomeruli and by immunofluorescence techniques. The results of the study emphasize the role of the reticuloendothelial system in the modulation of immune complex localization in the kidney and suggest a potential use of stimulants of the reticuloendothelial system in the therapy of immune complex nephritis.

Animals↗
PubMed1995

Reticuloendothelial system function in acute liver injury induced by D-galactosamine.

AIMS/METHODS: Reticuloendothelial system function, as assessed by clearance of radiolabelled bacteria, was evaluated in acute liver injury induced by D-galactosamine in rats, and compared with that after 70% liver resection model. RESULTS: Reticuloendothelial system function was significantly impaired in both instances, but the extent and the pattern of reticuloendothelial system impairment differed in the two models. While the elimination rate of the radiolabelled bacteria (k-value) decreased in both the liver resection and D-galactosamine groups (19% and 52%, respectively), the corrected phagocytic index (alpha) increased in 70% liver resection (247%), indicatine increased activity among the remaining reticuloendothelial system cells of the liver. Estimation of subserosal organ blood flow showed decreased flow to the cecum and distal small intestine (correction of intesting) in both groups, whereas it was significantly increased (477%) in the remaining parts of the liver in the liver resection group. CONCLUSIONS: These findings show that reticuloendothelial system activity is deranged in both these groups, which may explain the increased occurrence of bacterial complications observed in corresponding clinical conditions.

Animals↗