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M Constantin

Publications and source records attributed to M Constantin.

26 records · Page 2Linked to original sources
PubMedDate not supplied

Prolonged gastroprotective activity of a ranitidine-dextran conjugate.

The paper presents the influence of the ranitidine-dextran conjugate on the gastric secretion stimulated with carbachol on rats with a ligated pylorus [correction of ligaturated pilor]. The gastric lesions, the gastric juice volume and the total acidity at 6, 24 and 48 hours after the treatment were examined. Ranitidine serum content was determined by HPLC. Administration of the ranitidine-dextran conjugate produces a higher inhibition of gastric lesions at 48 hours than the administration of the free drug (61.4% versus 33.9%) and a prolonged action for more 48 hours. Synthesis of a macromolecular prodrug of ranitidine and its in vitro behavior was reported in a previous paper (11). The present paper studies the performances obtained in gastro-protective action by using the new ranitidine-dextran conjugate reported (11).

Animals↗
PubMedDate not supplied

Aminated polysaccharide microspheres as DNA delivery systems.

This article describes the production and characterization of cationic microparticles based on pullulan and starch for the delivery of nucleic acids. The microparticles were prepared by chemically cross-linkinking of a polymer solution dispersed in organic phase, followed by amination with N, N-diethyl-2-chloroethyl amine hydrochloride, or N-glycidyl-N,N-dimethyl-N-methylammonium chloride. The association of desoxyribonucleotide (DNA) with positively charged microparticles was determined. The association capacity and the affinity of microspheres for DNA were investigated as a function of type of polysaccharide, content and basicity of the amino groups. It was found that the both types of carriers synthetized display a high affinity for defibrotide due to the high porosity of polysaccharide microspheres (PMs). The in vitro release kinetics from microspheres showed an initial fast release of DNA (30 min) followed by slower release rate over 14 days. DNA release was influenced by the ionic strength of the receiving fluid. In addition, DNA release was slightly more rapid from pullulan than from starch complexes. DNA stability studies were performed by agarose gel, indicating no degradation even after 14 days. All the produced cationic microspheres were able to quantitatively load DNA. The release of DNA from PMs was strongly affected by the ionic strength of the receiving fluid. Finally, agarose gel electrophoresis of DNA released from microspheres indicated that no DNA degradation occurs even after 14 days of release from PMs.

Amination↗
PubMedDate not supplied

Chromosomal alterations in scleroderma.

To bring some new arguments in support of the genetic theory regarding the etiology and pathogenesis of scleroderma 12 patients (2 males and 10 females, ranging in age between 13 and 64 years) with both localized and systemic scleroderma were studied. For each patient chromosomal preparations were made in cell cultures from peripheral blood. The structural cytogenetic aberrations, observed in proportion of 81.81%, were, in the order of frequency: chromatid breakage, gaps, acentric fragments, deletions. The alterations appeared both in the systemic scleroderma and in the localized one but cannot represent a factor of prognosis for the disease. The association of Raynaud's syndrome with cytogenetic aberrations may lead to an early diagnosis of the disease.

Adolescent↗
PubMedDate not supplied

[Bepridil, a functional antagonist of beta1-adrenergic stimulation. Dissociated effects on cardiostimulation and lipolysis. (author's transl)].

1. Methods - In order to verify that the antagonism of isoprenaline by bepridil was not exclusive to cardiac receptors, anesthetized dogs were subjected to a double isoprenaline stimulation (two 15 minute perfusions at a rate of 1 microgram . kg-1 . min . -1 separated by a 75 minute interval). Bepridil at 5 mg . kg-1 was injected intravenously 45 minutes before the second isoprenaline stimulation, and compared to propranolol (1 mg . kg-1), practolol (5 mg . kg-1) and perhexiline (2.5 mg . kg-1). In addition, bepridil (1 mg . kg-1 . min . -1) and perhexiline (0.5 mg . kg-1 . min-1) were also perfused intravenously, simultaneously with the second isoprenaline stimulation. Classical cardiovascular parameters (heart rate, left dP/dt max., arterial pressure, coronary artery flow) together with plasma free fatty acid levels (FFA) were monitored at intervals of 5 minutes throughout the study. 2. Results - The two isoprenaline stimulations caused non-statistically different increases in the various parameters. All the cardiovascular effects of isoprenaline were inhibited by propranolol, except for the increase in coronary flow. Likewise, the increased plasma FFA level fell by 82.7 +/- 4.2% (p = 0.003). The tachycardia and elevated left dP/dt max. were antagonised by practolol, which the increased FFA levels fell by 64.3 +/- 4.8% (p less than 0.01). The other parameters were not altered. No signficant effect was observed with perhexiline. Rapid I.V. infection of bepridil only decreased the isoprenaline. induced tachycardia (from 74 +/- 15.6 syst. Min.-1 to 57.3 +/- 12.7 syst. min.-1). Perfusion of bepridil considerably limited the tachycardia, while moderately reducing the increased contractility later on. However, it had no effect on FFA levels or the other cardiovascular parameters. 3. Discussion and conclusions - The results obtained with propranolol and practolol are consistent with the competitive B-blocking activity of both compounds. The lack of effect noted in this instance with perhexiline may be explained by the recent hypothesis whereby this compound acts on the presynaptic nerve endings of the cardiac pacemaker system and depresses the release of endogenous noradrenaline while unable to antagonise exogenous adrenergic stimulation. The dissociated effects of bepridil with regard to cardiac and lipolytic stimulation by isoprenaline, strongly suggest functional antagonism by both compounds at cardiac level alone. This antagonism is explained by the depressant effects of bepridil on Ca2+/Na+ slow inward currents, as shown previously in myocardial preparations.

Adrenergic beta-Antagonists↗