Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sulfaguanidine”

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 19 recordsLinked to original sources
PubMed1990

Enhancing effect of pyrrolidone derivatives on the transdermal penetration of sulfaguanidine, aminopyrine and Sudan III.

The enhancing effect of pyrrolidone derivatives on the percutaneous penetration of sulfaguanidine, aminopyrine and sudan III was investigated using in vitro technique and excised rat skin. 1-Methyl (MP), 1-hexyl (HP) and 1-lauryl-2-pyrrolidone (LP) were used as penetration enhancers. Aminopyrine showed high penetration through skin although sulfaguanidine and sudan III showed little penetration. Pyrrolidone derivatives enhanced their penetrations. Especially HP and LP enhanced the penetration of sulfaguanidine to a high extent. Sudan III was not detected in the receptor phase regardless of the presence of enhancer. Pyrrolidone derivatives significantly increased the skin accumulation of sulfaguanidine, aminopyrine and sudan III. Penetration of pyrrolidone derivatives was also determined. MP and HP showed high penetrations. LP was not detectable in the receptor phase. MP, HP and LP showed high skin accumulations. These results suggested the usefulness of pyrrolidone derivatives as percutaneous penetration enhancers.

Administration, Cutaneous↗
PubMed2004

[Fixed drug eruption induced by sulfaguanidine].

INTRODUCTION: Fixed drug eruption is a lesion induced by drugs. The family of drugs usually incriminated are sulfonamides, tetracyclines and pyrazols. We describe nine cases of fixed drug eruption induced by sulfaguanidine, a sulfonamide with local action. CASE REPORTS: All the patients presented one or more fixed drug eruption reactivation lesions induced by sulfaguanidine as self-medication for diarrhea. The number of lesions increased in 7 cases after reactivation. The delay in occurrence of the fixed drug eruption decreased during the different episodes. The lesions predominated on the hands in 8 cases of 9. DISCUSSION: The sulfaguanidine must be added to the list of drug-induced fixed drug eruptions with limited absorption from the gastrointestinal tract.

Adolescent↗
PubMed1986

Gastrointestinal absorption of sulfaguanidine in neonatal and adult rats.

The pharmacokinetics of sulfaguanidine in rats was studied after its intravenous or oral administration. In adult rats, its elimination from plasma, after intravenous administration of 2.5 or 25 mg/kg doses, could be described by a two-compartment open model, while its plasma concentration after oral administration of 25 mg/kg doses, agreed with the one- or two-compartment open model. Neonatal rats displayed a lower elimination of sulfaguanidine than adult rats. Comparison of the drug's gastrointestinal absorption showed that the maximum plasma concentration after oral administration was significantly higher for neonatal than for adult rats. However, there was no significant difference between the times required to reach maximum plasma concentrations. The area under the plasma concentration-time curve at 0-infinity h was significantly higher for neonatal than for adult rats. The absolute bioavailability (57.86%) in neonatal rats was approximately five times that (12.76%) in adult rats. Thus, sulfaguanidine was poorly absorbed by adult rats, but was efficiently absorbed by immature gastrointestines of neonatal rats.

Absorption↗
PubMed1982

Effects of sulfaguanidine and amino acid imbalances on the induction of niacin deficiency in mature and immature Japanese quail (Coturnix coturnix japonica).

Effects of sulfaguanidine, leucine, or leucine plus isoleucine in a niacin free diet on body weight changes, liver weight, pyridine nucleotide concentrations, and activities of enzymes in mature female or immature Japanese quail were measured. The inclusion of .5% of sulfaguanidine or a high level of leucine in a niacin free diet had no influence during an 8-week period on liver pyridine nucleotide levels and the development of niacin deficiency symptoms in mature female quail. This would suggest that the mature female quail has a low requirement for dietary niacin. Immature quail were also tested to study the effects of amino acid imbalance on the induction of niacin deficiency. Although there was a marked reduction in body weight gains by the administration of leucine or leucine plus isoleucine, these treatments did not appear to accentuate niacin deficiency symptoms in these animals. Also pyridine nucleotide levels and malic enzyme, glyceraldehyde-3-phosphate dehydrogenase, and aldolase activities in liver tissues were not affected by these treatments.

Animals↗
PubMed1976

[Dynamics of agglutination in birds artificially infected with Salmonella gallinarum-pullorum and Salmonella typhimurium and treated with sulfaguanidine and furazolidone].

Canadian Leghorn chickens were used to study the effect of sulfaguanidine and furazolidon on the dynamics of blood agglutinin formation. The birds were artificially infected with Salmonella gallinarum-pullorum and Salmonella typhimurium. At various intervals following infection they were treated with sulfaguanidine 1% tablets and 0.04% furazolidon. The level of agglutinins was determined by the methods of Huddleson (whole blood agglutination reaction), the fast serum agglutination, the method after Wright, and the indirect hemagglutination reaction. It was found that the agglutinin level in birds treated in the course of ten days with the chemotherapeutics mentioned prior to their infection did not change. The use of these chemotherapeutics parallel to the infection of the test birds and ten days later inhibited agglutinin formation. This was more pronouncedly expressed in birds treated with furazolidon. The delayed use of these therapeutic means did not inhibit substantially the level of blood agglutinins.

Agglutinins↗
PubMed2005

Preparation, characterization and biological activity of Fe(III), Fe(II), Co(II), Ni(II), Cu(II), Zn(II), Cd(II) and UO(2)(II) complexes of new cyclodiphosph(V)azane of sulfaguanidine.

Novel hexachlorocyclodiphosph(V)azane of sulfaguanidine, H(4)L, l,3-[N'-amidino-sulfanilamide]-2,2,2,4,4,4-hexachlorocyclodiphosph(V)azane was prepared and its coordination behaviour towards the transition metal ions Fe(III), Fe(II), Co(II), Ni(II), Cu(II), Zn(II), Cd(II) and UO(2)(II) was studied. The structures of the isolated products are proposed based on elemental analyses, IR, UV-vis, (1)H NMR, mass spectra, reflectance, magnetic susceptibility measurements and thermogravimetric analysis (TGA). The hyperfine interactions in the isolated complex compounds were studied using 14.4keV gamma-ray from radioactive (57)Co (Mössbauer spectroscopy). The data show that the ligand are coordinated to the metal ions via the sulfonamide O and deprotonated NH atoms in an octahedral manner. The H(4)L ligand forms complexes of the general formulae [(MX(z))(2)(H(2)L)H(2)O)(n)] and [(FeSO(4))(2) (H(4)L) (H(2)O)(4)], where X=NO(3) in case of UO(2)(II) and Cl in case of Fe(III), Co(II), Ni(II), Cu(II), Zn(II) and Cd(II). The molar conductance data show that the complexes are non-electrolytes. The thermal behaviour of the complexes was studied and different thermodynamic parameters were calculated using Coats-Redfern method. Most of the prepared complexes showed high bactericidal activity and some of the complexes show more activity compared with the ligand and standards.

Anti-Bacterial Agents↗
PubMed1994

Fixed drug eruption caused by sulfaguanidine.

We report a patient who developed a fixed drug eruption (FDE) due to sulfaguanidine. This drug has not been previously implicated as a cause of FDE. The diagnosis was confirmed by an oral provocation and a biopsy of the lesion. Oral provocations with other sulfonamides, sulfamethoxazole and sulfadiazine, were well tolerated.

Administration, Oral↗
PubMed2000

Determination of hydration kinetics of sulfaguanidine anhydrate in aqueous solution by calorimetry.

A heat conduction microcalorimeter was used to evaluate the isothermal transition in water from anhydrate to monohydrate at 298 K. Sulfaguanidine (SGN) anhydrate was used as a model compound for the measurement of hydration kinetics in water. It is the well-known that SGN is very slightly soluble in water and capable of existing as the anhydrate or monohydrate form in the solid state. The transition rates of SGN anhydrate to monohydrate in tablets and granules were investigated. The hydration kinetics of tablets with controlled surface areas, obtained by coating the side with paraffin in aqueous solution, followed an apparent zero-order mechanism. On the other hand, the transition mechanism of the granules involved a phase boundary-controlled contracting interface reaction.

Calorimetry↗