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PubMed1993

Distribution of the nigropallidal neurons in the rat. (An experimental study using HRP and iron-dextran).

The distribution of nigral neurons retrogradely labelled from the globus pallidus was studied in 9 rats using the horseradish peroxidase and the iron-dextran labelling technique. Retrogradely labelled neurons significantly prevailed in the ipsilateral substantia nigra pars compacta. Labelled neurons localized in the ipsilateral substantia nigra pars compacta were demonstrated throughout the anteroposterior extent of the nucleus and prevailed in its lateral half. A small number of labelled neurons was found in the lateral part of the ipsilateral substantia nigra pars reticulata, in the ipsilateral ventral tegmental area and in the contralateral substantia nigra pars compacta. A considerable perikaryal polymorphism and differences in the size are characteristic of the nigral neurons labelled from the globus pallidus.

Animals↗
PubMed1995

Absorption of iron dextran from the peritoneal cavity of rats.

We investigated the absorption rate and acute toxicities of intraperitoneal iron dextran in rats. Eighteen Sprague-Dawley rats were divided into three groups (n = 6). The animals were given standard 1.5% Dianeal (group 1) or 1.5% Dianeal containing iron in a concentration of 2 mg/L (group 2) or 10 mg/L (group 3) as iron dextran. First, a predialysis blood sample was obtained, and 25 mL of the designated dialysis solution was instilled into the peritoneal cavity. After a 6-hour cycle the dialysate was drained, and a postdialysis blood sample and specimen of the peritoneum were obtained. The iron concentrations of the dialysis solution, the dialysate, and both serum samples were determined. Histological samples were processed by hematoxylin and eosin and Prussian blue stain. Results of the iron concentration (mg/L) of the dialysis solution, the dialysate, and the percent of the absorbed iron were as follows: group 1: 0.00, 0.20 +/- 0.15, N/A; group 2: 2.24, 0.66 +/- 2.8, 73.8 +/- 11.0; group 3: 9.84, 2.12 +/- 0.62, 80.8 +/- 5.7. The serum iron concentration did not change. No abnormal findings were found histologically. More than 70% of the iron dextran was absorbed from the peritoneal cavity of the rats during a 6-hour peritoneal dialysis exchange. Intraperitoneal iron dextran may be an alternative route of iron delivery.

Absorption↗
PubMed1995

The efficacy of iron dextran for the treatment of iron deficiency in hemodialysis patients.

We prospectively evaluated the efficacy of intravenous iron dextran for the replacement of iron stores in iron deficient hemodialysis patients. Twenty-eight patients with serum ferritin < 100 ng/ml were treated with 100 mg intravenous iron dextran for ten consecutive hemodialysis treatments. Therapy was considered successful if the serum ferritin remained > 100 ng/ml for 4 months after treatment. Mean hematocrit increased from 29.1 +/- 0.9% at baseline to 33.6 +/- 1.8% at ten weeks (p < 0.05). The mean erythropoietin dose decreased from 94.1 +/- 5.3 U/kg body weight per treatment at baseline to 82.6 +/- 4.4 U/kg body weight per treatment at 10 weeks (p < 0.05). The mean serum ferritin at baseline was 38.3 +/- 5.5 ng/ml, at 2 weeks 135.9 +/- 19.7 ng/ml, at 6 weeks 114.1 +/- 22.4 ng/ml, and 86.6 +/- 17.7 ng/ml at 10 weeks. The number of patients at the therapeutic target (serum ferritin > 100 ng/ml) was 13 of 28 at 2 weeks after therapy, 9 of 28 at 6 weeks, and 8 of 28 at 10 weeks. The initial serum ferritin was the variable most predictive of successful therapy. None of 15 patients with baseline serum ferritin less than 28 ng/ml had a serum ferritin > 100 ng/ml at 4 months, compared with 8 of 13 (61%) with initial ferritins > or = 28 ng/ml. Baseline hematocrit and transferrin saturation were not predictive of therapeutic success. In summary, this regimen for administration of intravenous iron dextran resulted in improved erythropoiesis, however, at study completion iron stores remained inadequate in the majority of patients. Baseline serum ferritin < 28 ng/ml was highly predictive of patients who failed to reach the therapeutic target.

Anemia↗
PubMedDate not supplied

Falsely decreased total serum calcium concentration associated with iron dextran injection.

We cared for a patient in whom iron dextran administration interfered with the determination of total serum calcium concentration. An unexpected elevation in serum phosphorus concentration also occurred after the iron dextran infusion. A MEDLINE search from 1966 to present was conducted, and the manufacturer of the iron dextran was contacted for information related to these findings. Several drugs and diseases were found that may decrease serum calcium and increase phosphorus concentrations. We found one anecdotal citation of iron dextran interfering with serum calcium concentrations, but no reports of interference with serum phosphorus concentrations. Doses of iron dextran in excess of 250 mg may cause a false decrease in total calcium concentration more than 4 hours after the infusion is completed. A false increase in serum phosphorus concentrations after the infusion requires further investigation.

Antiviral Agents↗
PubMed1977

Enhancement of survival in acute experimental fowl typhoid in chicks by the administration of iron dextran.

Chicks aged 15 days were infected orally with 10(6-4) living Salmonella gallinarum. Iron from iron dextran or ferric ammonium citrate (DFe and CFe respectively), in doses of 2-0 or 0-4 mg/kg given intramuscularly at the time of infection, had no effect on subsequent mortality compared with infected controls. Increasing the amount of CFe to the maximum (20 mg/kg) that was non-toxic intramuscularly was also ineffective but when the dose of DFe was increased to 20 or 50 mg/kg the survival rate rose sharply. If given at other times in relation to the time of infection, or more frequently, 50 mg/kg or more of DFe was less active. The increased survival rate among infected chicks given 50 mg/kg of DFe at the time of infection was accompanied by decreases in the severity of the morbid changes in the disease, and by reductions of between c 10- to 100-fold in the numbers of viable S gallinarum in the liver, spleen or blood at the height of the acute infection. DFe (50 mg/kg) given at the time of infection also eliminated the difference in the survival rate noted previously between infected chicks fed respectively with diets containing fish or meat meal as the sole source of supplementary protein.

Anemia↗
PubMed1977

Cellular distribution of orally and intramuscularly administered iron dextran in newborn piglets.

Histochemical studies were performed on tissues from piglets of different ages treated orally with iron dextran soon after birth. The mucosal cells in the distal region of the small intestine were heavily laden with stainable iron granules during the first three days after the iron administration. The absorptive epithelial cells are desquamated within seven to ten days after birth. Consequently, the number of iron granules gradually diminishes during the first seven days after treatment and no iron granules are demonstrated 12 days after the administration of iron. The iron dextran complex is pinocytosed in newborn piglets and then transported via the lymphatic system. Thus the sinusoidal lining cells of the body and mesenteric lymph nodes are already heavily laden with iron granules 24 hours after oral treatment. This iron store is released only slowing during the first weeks of life. Great amounts of iron granules are demonstrated in the liver and spleen macrophages during the first week after the administration of iron. Due to the rapid utilization of iron in growing piglets these iron stores diminish sharply during the weeks following birth. The distribution of stainable iron in the lymph nodes, liver and spleen seven days after intramuscular injection of iron dextran in newborn piglets was comparable to that for oral administration at that stage of the experiment.

Administration, Oral↗
PubMed1979

Endotoxin determination in viscous opaque solutions of iron dextran by Limulus amebocyte lysate.

LAL would not form a clot when mixed with a viscous, opaque parenteral preparation of iron dextran spiked with endotoxin. However, recoverable precipitate could be obtained by diluting the LAL iron dextran mixture with PBS and centrifuging. Although the pellet so formed was red colored the protein present could be quantitated by dissolving it in a Coomassie Blue stain solution. The very rapid change in color from reddish black to deep blue was measured quantitatively in a spectrophotometer and was sigmoidally related to the amount of endotoxin used to spike the iron dextran. This method is suggested to be generally useful to measure quantitatively endotoxin concentrations too low to form a clot with LAL but high enough to precipitate recoverable protein from LAL.

Animals↗
PubMed1976

Intravenous iron-dextran therapy in the treatment of anemia occurring in surgical, gynecologic and obstetric patients.

An infusion of iron-dextran diluted in 1,000 milliliters of physiologic saline solution was given to 51 patients. The average hemoglobin response was 1.9 grams per deciliter per week. Mean corpuscular volume, mean corpuscular hemoglobin concentration and mean corpuscular hemoglobin deficits also were corrected. There were no allergic reactions. This is an extremely reliable and safe method of replenishing depleted iron in patients.

Adolescent↗
PubMed1994

Immunologic studies of anaphylaxis to iron dextran in patients on renal dialysis.

Systemic reactions resembling anaphylaxis have occurred after intravenous (IV) iron-dextran administration, a treatment modality that has acquired increased acceptance following the use of erythropoietin for the anemia of patients with chronic renal diseases. Three such patients sustained anaphylactoid reactions immediately after receiving IV test doses of iron-dextran which were their only known exposures. In an effort to determine the mechanism of their reactions, we applied tests for (1) basophil degranulation by iron-dextran, basophil histamine release; (2) a type I anaphylactic reaction, specific IgE antibodies; and (3) an immune complex activation, specific IgG antibodies against iron-dextran. Six other patients with renal diseases served as controls, three of whom had tolerated IV iron-dextran, and three without known exposure. One patient only had any test abnormalities. Her initial positive basophil histamine release and specific IgG antibodies reversed and declined respectively at a 4-month follow-up study. She had developed anaphylaxis, and her studies had been performed at a time after anaphylaxis earlier than the other two. The mechanisms of iron-dextran anaphylaxis may be multiple and not be detectable several months after the incident. Prospective studies will probably be required for a predictive test to be developed.

Adult↗
PubMed1990

Thalamic afferents from the brain stem. An experimental study using retrograde single and double labelling with HRP and iron-dextran in the rat. II. Nucleus laterodorsalis and subnucleus compactus nuclei pedunculo-pontini.

The reticulo-thalamic projection arising from the ncl. latero-dorsalis and from the subncl. compactus nuclei pedunculo-pontini was studied in single and double experiments using 51 injections of HRP and/or iron-dextran. The ncl. latero-dorsalis projects to the midline nuclei, to the ncl. mediodorsalis and to the ncl. ventralis lateralis, and, together with the subncl. compactus, also to the anterior, intralaminar nuclei, to the ncl. ventralis basalis and ncll. posteriores. Part of the substantia grisea centralis pontis adjoining the oral pole of the ncl. latero-dorsalis sends out fibres throughout the region of the above listed nuclei while projecting only scantily to the anterior nuclei and to the ventrobasal complex. The projection from the ncl. laterodorsalis has a major contralateral component (about one third of the labelled cells) whereas the contralateral component arising from the subncl. compactus is very scanty. We found no topographic arrangement in the projection (though there were signs of a crude mediolateral organization). The projection, mainly from the ncl. latero-dorsalis, shows relatively dense collateralization (double-labelled cells): ipsi- as well as contralaterally to the intralaminar nuclei, or collaterals to the ipsilateral intralaminary nuclei and, at the same time, to the contralateral ncl. mediodorsalis. A similar, albeit smaller collateralization, was also seen in the ncl. pedunculo-pontinus, its subncl. compactus: ipsilateral collateralization between the anterior and intralaminar nuclei or between the anterior and posterior intralaminar nuclei of the ipsilateral side.

Animals↗
PubMed1993

[Iron deficiency anemia is not always simple].

BACKGROUND: Malabsorption of oraliron is rare, and more frequently suspected than proved. It could be due to prolonged iron deficiency. CASE REPORTS: Case no. 1: A boy was admitted at the age of 5 months for recurrent bronchitis. His hemoglobin was 8.2 g/dl, mean corpuscular volume (MCV) 60 micron3, mean corpuscular hemoglobin (MCH) 15 ng and mean corpuscular hemoglobin concentration (MCHC) 25 gHb/dl. The serum iron was 1 microgram/dl, iron binding capacity (IBC) was 284 micrograms/dl and ferritin was 14.9 ng/ml. Dietary iron was inadequate. The patient was given ferrous sulfate but iron deficiency persisted at the ages of 11 months and 3 years, probably due to poor compliance. Similar hematologic data (Hb: 6.4 g/dl, MCV 55 micrograms/m3, MCH 13.9 ng, MCHC 24 gHb/dl) were found at the age of 9 years. The patient was then given ferrous sulfate orally as test but the serum iron levels were unchanged during the 4 hours following ingestion. A parenteral iron preparation (iron-dextran, 500 mg) improved the hematologic data. 6 months later, a new oral test with ferrous sulfate improved the serum iron level. Case no. 2: A boy with complex congenital cardiopathy was operated on in the neonatal period and given oral iron at the age of 9 months because of anemia with microcytosis and hypochromia. This anemia was still present at 17 months and was associated with normal or high serum ferritin. Electrophoresis of hemoglobin was normal. At the age of 4 yr 5 mo, Hb was 9.7 g/dl, MCV 62.8 micrograms/m3, MCH 18.4 ng, iron 16 micrograms/dl and ferritin 94.1 ng/ml. An oral test with ferrous sulfate failed to increase the serum iron. The patient was then given parenteral iron-dextran without benefit, and a second oral test remained ineffective. After a second course of parenteral iron-dextran, Hb was 11.5 g/dl, MCV 74.1 micrograms/m3, MCH 23.7 ng while the serum iron remained low (23 micrograms/dl) and ferritin increased to 587 ng/ml. A third oral test with ferrous sulfate was still ineffective, as was a test using 4 mg/kg iron. CONCLUSION: The first patient suffered from iron malabsorption, presumably due to iron deficiency. The second patient could have abnormal metabolism and/or abnormal ferritin.

Anemia, Hypochromic↗
PubMed1991

The effect of ligands on the uptake of iron by cells in culture.

Uptake of iron by a mammalian epithelial cell line (CNCM I-221) was shown to be dependent on the nature of the iron complex. Iron uptake was demonstrated by cytochemical staining and determination of redox-reactive iron in cell lysates. Three classes of ligands were investigated: (i) low molecular weight hydrophilic compounds, represented by ethylenediamine-tetraacetic acid (EDTA) and other charged ligands such as adenosine phosphates (ATP, ADP, AMP) and diethylenetriaminepentaacetic acid (DTPA), (2) low-molecular weight lipophilic ligands such as 8-hydroxyquinoline (8-HQ) and (3) a high molecular mass ligand, dextran. Iron complexed to 8-HQ accumulated intracellularly, the uptake rate of iron being 4.16 fmoles cell-1 h-1 of exposure at 37 degrees C or 3.86 fmoles cell-1 h-1 at 4 degrees C. Iron-dextran was endocytosed and retained in phagosomes. The uptake rate of iron following exposure to iron dextrans was found to be 5.6 fmoles cell-1 h-1 of exposure at 37 degrees C. In contrast to iron/8-HQ, uptake of iron dextran by cells was inhibited at 4 degrees C. Iron complexed to low molecular weight hydrophilic ligands was not taken up by cells. Cytotoxicity was measured by reduction of plating efficiency or tritiated thymidine incorporation. These tests showed that toxic effects of added iron were demonstrable only in cells exposed to the complex with 8-HQ.

Adenosine Diphosphate↗
PubMed1988

Studies on haemosiderin and ferritin from iron-loaded rat liver.

Haemosiderin has been isolated from siderosomes and ferritin from the cytosol of livers of rats iron-loaded by intraperitoneal injections of iron-dextran. Siderosomal haermosiderin, like ferritin, was shown by electron diffraction to contain iron mainly in the form of small particles of ferrihydrite (5Fe2O3.9H2O), with average particle diameter of 5.36 +/- 1.31 nm (SD), less than that of ferritin iron-cores (6.14 +/- 1.18 nm). Mössbauer spectra of both iron-storage complexes are also similar, except that the blocking temperature, TB, for haemosiderin (23 K) is lower than that of ferritin (35 K). These values are consistent with their differences in particle volumes assuming identical magnetic anisotropy constants. Measurements of P/Fe ratios by electron probe microanalysis showed the presence of phosphorus in rat liver haemosiderin, but much of it was lost on extensive dialysis. The presence of peptides reacting with anti-ferritin antisera and the similarities in the structures of their iron components are consistent with the view that rat liver haemosiderin arises by degradation of ferritin polypeptides, but its peptide pattern is different from that found in human beta-thalassaemia haemosiderin. The blocking temperature, 35 K, for rat liver ferritin is near to that reported, 40 K, for human beta-thalassaemia spleen ferritin. However, the haemosiderin isolated from this tissue, in contrast to that from rat liver, had a TB higher than that of ferritin. The iron availability of haemosiderins from rat liver and human beta-thalassaemic spleen to a hydroxypyridinone chelator also differed. That from rat liver was equal to or greater, and that from human spleen was markedly less, than the iron availability from either of the associated ferritins, which were equivalent. The differences in properties of the two types of haemosiderin may reflect their origins from primary or secondary iron overload and differences in the duration of the overload.

Animals↗