Biomedical subjects

R Santonja

Publications and source records attributed to R Santonja.

11 recordsLinked to original sources

PubMed1987

Effects of subinhibitory concentrations of pefloxacin on the adherence of Staphylococcus aureus to human cells.

The adherence of bacterial strains to eukaryotic cells can be influenced by subinhibitory concentrations of antibiotics. The effect of sub- and infra-MICs of pefloxacin, a new broad-spectrum antibacterial quinolone, on the adherence of Staphylococcus aureus to human buccal cells, was studied. Six S. aureus strains belonging to several serotypes and all sensitive to pefloxacin were pretreated with serial twofold dilutions of the drug (from 1/2 to 1/1024 the MIC). After the adhesion test, 100 buccal cells were counted in randomly chosen microscopic fields using a Nomarski interference microscope and attachment was measured as the percentage of cells with at least 50 or more adhering bacteria. Sub-MICs (1/2 and 1/4 the MIC) of pefloxacin increased the diameter of the six staphylococci. All of the strains, grown in the presence of pefloxacin, exhibited a markedly altered capacity for adhesion to buccal cells. The highest significant decrease was observed for 1/2 to 1/8 the MIC, although infra-MICs such as 1/1024 the MIC also decreased the attachment of S. aureus to buccal cells. These results were compared with those obtained with other antibiotics active against S. aureus.

Anti-Bacterial Agents↗

PubMed1983

[Comparative study of platelet anti-aggregation effect of several anti-inflammatory agents].

The relationships between inflammation and platelets, particularly between inflammation and platelet aggregation, have been elucidated during the last two years. Platelet aggregation is greatly enhanced by PGE2 and PGF2 alpha prostaglandins, which act as mediators of inflammation through the part they play in the regulation of platelet cyclic AMP whose intracellular concentration is determined by PGE1. Recently, acetylsalicylic acid and indomethacin have been shown to inhibit the synthesis and release of PGE2 as well as platelet aggregation. These findings prompted the present study of the inhibitory effect on platelet aggregation of two antiinflammatory drugs, metiazinic acid and ketoprofen. Indomethacin was elected as the reference drug. Both agents studied inhibit platelet aggregation more strongly than indomethacin. Inhibition of the release reaction is significantly stronger with ketoprofen than with the reference drug. The authors believe that this in vitro trial, in which platelet aggregation is induced by collagen, is of special significance as it involves the same biologic phenomena as those which occur in vivo.

Adenosine Diphosphate↗

PubMed1983

Plasma binding of an alpha-blocking agent, nicergoline--affinity for serum albumin and native and modified alpha 1-acid glycoprotein.

The binding of nicergoline, an alpha-blocking drug, by human plasma proteins was studied using gel filtration, polyacrylamide gel electrophoresis, and equilibrium dialysis techniques. 3H-labeled nicergoline added to plasma was eluted together with two major protein fractions, one containing mainly serum albumin, the other glycoproteins such as alpha 1-acid glycoprotein (alpha 1-AG). Equilibrium dialysis experiments with pure human serum albumin and alpha 1-AG as well as with its chemically modified forms, desialylated, carboxymethylated, and both desialylated and carboxymethylated alpha 1-AG gave the following results: nicergoline has about a 4-fold higher affinity for alpha 1-AG than for serum albumin. There are two binding sites per molecule on serum albumin and one on alpha 1-AG. The binding parameters of alpha 1-AG were not significantly modified by desialylation or carboxymethylation. Only desialylated and carboxymethylated alpha 1-AG showed a decreased binding for nicergoline, suggesting conformational modifications induced by these combined treatments. The fact that desialylated alpha 1-AG keeps its affinity for nicergoline suggests the possibility of a selective introduction of this drug in cells possessing the Ashwell-type specific receptor for desialylated alpha 1-AG, for instance hepatocytes. Increased serum alpha 1-AG concentration induced by inflammatory reactions will also modify the distribution of bound nicergoline between serum albumin and alpha 1-AG and as a consequence its half-life and cell distribution.

Binding Sites↗

PubMed1980