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Is it true that cardiac operations with cardiopulmonary bypass impair the reticuloendothelial system?

Reticuloendothelial system (RES) function after cardiac operations is a controversial issue. Sequential changes in plasma fibronectin levels and RES phagocytic function were studied after a cardiac operation and a lung operation (control). In the cardiac operation group, the plasma fibronectin level decreased until the third postoperative day and increased thereafter. Reticuloendothelial system phagocytic function remained unchanged on the third postoperative day and then it increased. However, in the control group it increased significantly after operation. In the past, investigators have demonstrated a decline in plasma fibronectin levels following cardiac operation and have assumed that RES function was impaired. However, this sequential study showed that phagocytic function was not impaired, but its enhanced phase was delayed. Moreover, our previous morphologic studies demonstrated that RES function was potentially activated after cardiopulmonary bypass. It appears that the delay of the enhanced phase is caused by the overloading of substances which must be processed by the RES during cardiopulmonary bypass. Thus, we conclude that cardiac operation produces hyperactive, yet oversaturated RES function. There is no impairment of RES function after cardiac operations.

Adult↗

Interactions of liposomes with the reticuloendothelial system. Effects of reticuloendothelial blockade on the clearance of large unilamellar vesicles.

Large unilamellar liposomes (also called reversed phase vesicles or REVs) composed of DPPC and cholesterol are cleared from the circulation of the rat by a process which closely resembles the clearance of colloidal particles by the reticuloendothelial system. Thus, increasing the total amount of REVs administered by giving a loading dose of unlabelled REVs slows the clearance of a test dose of radioactively labelled REVs. This resembles the reticuloendothelial 'blockade' induced by large doses of colloids. Administration of other types of particles known to induce reticuloendothelial blockade, such as latex beads and xenogeneic red cells, also slows the clearance of radioactively labelled REVs. Administration of small unilamellar liposomes (SUVs) can also cause blockade of REV clearance, but the onset of blockade is delayed until a substantial fraction of the SUVs have been removed from the circulation. Blockade caused by the administration of large doses of REVs seems to result from a direct action on reticuloendothelial cells rather than from depletion of opsonic factors in the blood. Partial blockade of REV clearance produces a modest alteration of the tissue distribution of REVs, with enhanced uptake in the lungs. These results suggest that both REVs and SUVs are taken up by the reticuloendothelial system via a process which closely resembles the clearance of other types of colloids.

Animals↗

Rates of systemic degradation and reticuloendothelial system (RES) uptake of thermosensitive liposome encapsulating cisplatin in rats.

The systemic degradation and reticuloendothelial system (RES) uptake of cisplatin (CDDP)-encapsulated thermosensitive liposomes composed of dipalmitoylphosphatidylcholine (DPPC) and distearoylphosphatidylcholine (DSPC) (DPPC/DSPC = 9/1, 7/3, and 5/5, w/w) after intravenous administration to rats were examined by measuring the platinum (Pt) levels in the blood and RES (liver and spleen). The blood liposome level profile showed first-order rate elimination for each liposome administration. The elimination rate (Kel) was faster when the content of DSPC was lower (Kel: 1.3/hr for 9/1-liposomes, 0.7/hr for 7/3-liposomes, 0.5/hr for 5/5-liposomes). On the other hand, the RES liposome level profile showed distribution of liposomes followed by elimination therefrom. The RES level of the liposomes was lower when the content of DSPC was smaller (maximal level: 25% for 9/1-liposomes at 1 hr, 32% for 7/3-liposomes at 1 hr, 37% for 5/5-liposomes at 2 hr). The kinetic analysis demonstrated that the RES uptake rate (Kres) was almost the same among the liposomes (0.4/hr), while the systemic degradation rate (Kdeg; Kel-Kres) became larger as the content of DSPC decreased (0.9/hr for 9/1-liposomes, 0.3/hr for 7/3-liposomes, and 0.1/hr for 5/5-liposomes) and that the RES liposome distribution amount was dependent not only on the Kres but also on the Kdeg and the rate of RES liposome degradation. The Kdeg for each type of liposome corresponded with the systemic CDDP release rate.

Animals↗

[Reliability of the lipid emulsion test for reticuloendothelial system].

The reticuloendothelial system is important as one of the self defense mechanisms. We performed two investigations to confirm the reliability of the lipid emulsion test for determining the reticuloendothelial system function. 1) The lipid emulsion serum clearance was contrasted with the counts of lipid emulsions phagocytosed by Kupffer cells in liver. 2) Lipid emulsion clearance was contrasted with the hepatic uptake rate of 99mTc-phytate. The result demonstrated a positive correlation among lipid emulsion clearance, the counts of lipid emulsions phagocytosed by Kupffer cells and the hepatic uptake rate of 99mTc-phytate. These results confirm that the lipid emulsion test is sufficient to reflect Reticuloendothelial system function.

Adult↗

Rates of systemic degradation and reticuloendothelial system uptake of calcein in the dipalmitoylphosphatidylcholine liposomes with soybean-derived sterols in mice.

The systemic degradation and the reticuloendothelial system (RES) uptake of calcein entrapped in dipalmitoylphosphatidylcholine (DPPC) liposomes with soybean-derived sterols (SS) were examined after intravenous administration to mice by measuring the free and liposomal calcein levels in the blood. The results indicate that the rates of systemic degradation and the RES uptake of liposomes decrease with the addition of SS in DPPC liposomes since the SS has the ability to stabilize the liposomes. The rate of uptake by RES is larger than the rate of systemic degradation. The rate of leakage of calcein from liposomes by incubation in plasma in vitro is almost the same as that of systemic degradation in vivo.

1,2-Dipalmitoylphosphatidylcholine↗

Cellular aging of the reticuloendothelial system.

The reticuloendothelial system (RES) consists of macrophages and other endocytic cells which contribute to natural resistance to disease agents. The RES has been implicated as being partly responsible for the observed age-related decrease in resistance to pathogenic microorganisms in man and experimental animals. It is largely unknown to what extent age-related deficiencies in specific functions of reticuloendothelial cells contribute to the decrease of RES functions. This study describes experiments focussed on Kupffer and endothelial cells of the liver which represent a major part of the RES and are primarily responsible for clearance of potentially harmful substances from the circulation. The age-related changes in the clearance of a RES test colloid (heat-aggregated colloidal albumin (CA)) and of E. coli endotoxin were investigated using female BN/BiRij rats of various age groups. With CA, studies were performed on the plasma clearance and on the endocytic capacity of whole liver and of Kupffer and endothelial cells in vivo, as well as on the kinetics of endocytosis by Kupffer cells in culture. The results showed that the plasma disappearance of endotoxin was significantly prolonged in rats of 24 and 36 months resulting in an increase in half-life of about 50% as compared to young rats. The plasma clearance of CA, the uptake by the liver and the endocytosis by endothelial cells were unchanged with age. In contrast, an age-related decrease in endocytic capacity was observed in Kupffer cells in vivo and in Kupffer cells which were isolated from rats of various ages and maintained in culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

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↗

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↗

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↗

[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↗

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↗

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↗