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Biomedical subjects

J Migne

Publications and source records attributed to J Migne.

At least 19 recordsLinked to original sources
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

[Action of ketoprofen on hepatic lysosomes in the rat].

Evidence for the stabilizing effect of ketoprofen on the lysosomal membrane is presented. Ketoprofen was as potent as indomethacin in stabilizing lysosomes subjected to changes in osmotic pressure. This effect was more marked in rats with adjuvant arthritis than in normal animals.

Animals↗
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↗
PubMed1979

[Ultrastructural study on the effect of an inhibitor of platelet aggregation (author's transl)].

10-Methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) is introduced into human platelet-rich plasma at different stages of collagen-, ADP- or epinephrine-induced aggregation. Ultrastructural fixation is processed while aggregation on the same plasma sample is recorded. If introduced before the aggregating agent, nicergoline completely neutralises its action and the platelets become spherical. The microtubule marginal bundle is disorganized and both open and dense canalicular systems are modified. If intoduced after the aggregating agent, nicergoline immediately stops the aggregation and disaggregation follows, with complete separation of the platelets. Morphology of microtubules and canalicular systems depend on the time before application of nicergoline. Nicergoline stops the induction of aggregation as well as ADP release. Disaggregation is an active process involving the microtubules.

Blood Platelets↗
PubMed1977

[Complications following cementing of joint prosthesis].

The authors studied changes in the level of lactate dehydrogenase during insertion of hip prostheseis fixed with methyl methacrylate cement. Thirty patients were studied here. In 23 of them, the L.D.H. isoenzymes were estimated. The variations in these enzymes appear 3 hours after the second fixation with cement: rise in L.D.H., isoenzyme 5, (of skeletal muscle origin) of isoenzymes 3 and 4, (of pulmonary origin). This is a sign of pulmonary involvement even in the absence of clinical signs.

Adult↗
PubMed1976

Action of ketoprofen on hepatic lysosome in the rat.

Evidence for the stabilizing effect of ketoprofen on the lysosomal membrane is presented. Ketoprofen was as potent as indomethacin in stabilizing lysosomes subjected to changes in osmotic pressure. This effect was more marked in rats with adjuvant arthritis than in normal animals.

Animals↗