Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Dimercaprol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources

Renal tubular secretion of the alkanesulfonate 2,3-dimercapto-1-propanesulfonate.

The in vivo tubular secretion and metabolism of 2,3-dimercapto-1-propanesulfonate (DMPS) was examined in the chicken by use of the Sperber technique. Infusion of DMPS into the renal portal circulation of the chicken at rates equal to or less than 7.5 mumol X min-1 X kg body wt-1, resulted in a tubular excretion ratio of 0.5 for DMPS with 90% of the infused DMPS excreted in the urine unchanged. Renal tubular secretion accounted for approximately 90% of the total DMPS excreted into the urine during the infusion of DMPS at a rate of 0.75 mumol X min-1 X kg-1. The secretion of DMPS was saturable and was inhibited by p-aminohippurate (PAH), probenecid, and heptanesulfonate. Taurine (2-aminoethanesulfonate), isethionate (2-hydroxyethanesulfonate), and 2-mercaptoethanesulfonate had no effect on the secretion of DMPS or PAH. Renal tubular secretion may explain several pharmacological characteristics previously reported for DMPS, including the selective removal of heavy metals from the kidney.

Alkanesulfonates↗

Complexing activity and excretion of 2,3-dimercapto-1-propane sulfonate in rat kidney.

The renal handling of the heavy metal complexing agent, 2,3-dimercapto-1-propane sulfonate (DMPS), was examined in the isolated perfused rat kidney (IPRK). Net tubular secretion of DMPS was saturable and blocked by p-aminohippuric acid (PAH) and probenecid (PRB), indicating involvement of carrier-mediated transport in the excretion of DMPS. DMPS was oxidized to a disulfide form (DMPSS) in perfusate and reduced to a sulfhydryl form (DMPSH) in kidney. In kidneys isolated from rats pretreated with HgCl2, DMPS produced a dose-dependent decrease in retention of inorganic mercury, an increase in urinary excretion of mercury, and an increase in the amount of mercury transferred from kidney into venous perfusate. At a maximally effective dose, 40% of the renal mercury content was excreted in urine during 30 min of perfusion. Urinary excretion of mercury induced by DMPS was completely blocked by concentrations of PRB that blocked tubular secretion of DMPS and decreased uptake of DMPS in kidney. Thus tubular secretion of DMPS and reduction of DMPSS to DMPSH are important in the renal handling of DMPS and may contribute to the activity of DMPS as a complexing agent for renal mercury.

Animals↗

Effect of glucocorticosteroid treatment on ovalbumin-induced IgE-mediated immediate and late allergic response in guinea pig.

The effect of glucocorticosteroid (GCS) treatment on ovalbumine-induced IgE-mediated immediate and late allergic response was studied in sensitized guinea pigs. The results show that the GCS budesonide (BUD) inhibits the allergen-induced IgE-mediated immediate and late bronchial obstruction. The effect on the early reaction is correlated to the inhibition of leukotrienes and histamine release. The importance of mediator release inhibition for the antianaphylactic effect of GCS is discussed. In examining the effect on the late reaction, it was found that BUD had to be present during the early reaction but did not inhibit the early reaction. Furthermore, the effect on the late reaction was correlated to the inhibition of vascular leakage but not to the infiltration of inflammatory cells as examined in bronchoalveolar lavage. The results indicate that some triggering factors important for the development of the late reaction are released during the early reaction. Inhibition of the release of that factor or the activation of inflammatory cells by that factor might be the mechanism behind the antiinflammatory activities of GCS.

Anaphylaxis↗

Modulation of airway inflammation in cystic fibrosis. In vivo suppression of interleukin-8 levels on the respiratory epithelial surface by aerosolization of recombinant secretory leukoprotease inhibitor.

Based on the knowledge that neutrophil elastase (NE) in cystic fibrosis (CF) epithelial lining fluid (ELF) can induce human bronchial epithelial cells to express the gene for interleukin 8 (IL-8), an 8.5-kD neutrophil chemoattractant, we have evaluated CF ELF for the presence of IL-8, and investigated the ability of aerosolized recombinant secretory leukoprotease inhibitor (rSLPI) to suppress NE, and hence IL-8, levels on the respiratory epithelial surface in CF. Enzyme-linked immunoassay revealed 21.9 +/- 4.8 nM IL-8 in CF ELF compared with none in normals. Active NE was detectable in ELF of all individuals with CF and was significantly decreased (P < 0.03) after aerosolization of rSLPI. Human bronchial epithelial cells exposed to CF ELF recovered before rSLPI therapy expressed IL-8 mRNA transcripts, but ELF recovered after rSLPI therapy induced far less bronchial epithelial cell IL-8 gene expression. Consistent with this, rSLPI aerosol therapy caused a marked reduction in CF ELF IL-8 levels (P < 0.05) and neutrophil number (P < 0.02). There was also a clear association between CF ELF active NE and IL-8 levels (r = 0.94). These data suggest that rSLPI therapy not only suppresses respiratory epithelial NE levels, but also breaks a cycle of inflammation on the CF epithelial surface.

Adult↗

Neonatal lead poisoning. An unusual clinical manifestation.

A case of lead encephalopathy in a 2-month-old child is reported. Modes of poisoning are discussed and the unusual clinical manifestations of metallic brownish discoloration of nails and subdural effusion are presented. The possibility of lead poisoning as a cause of convulsions in neonates should be considered by doctors caring for these patients. Detailed history of lead exposure in prenatal and postnatal periods aids in early diagnosis and treatment which, thus, prevent severe neurological sequelae.

Adult↗