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R Lisciani

Publications and source records attributed to R Lisciani.

12 recordsLinked to original sources
PubMed1992

Effect of prolonged treatment with propionyl-L-carnitine on erucic acid-induced myocardial dysfunction in rats.

The aim of this study was to evaluate the ability of propionyl-L-carnitine to prevent cardiac damage induced by erucic acid. Rats were fed for 10 days with normal or 10% erucic acid-enriched diets with or without propionyl-L-carnitine intraperitoneally injected, (1 mM/kg daily, for 10 days). The erucic acid diet produced increases in triglycerides (from 5.6 to 12.4 mg/gww, P less than 0.01), and free fatty acids (from 2.0 to 5.1 mg/gww, P less than 0.01), but no changes in phospholipids. When the hearts were perfused aerobically with an isovolumic preparation there was no difference in mechanical activity. On the contrary, when pressure-volume curves were determined, the pressure developed by hearts from the erucic acid-treated rats were reduced. Independent of diet, propionyl-L-carnitine treatment always produced positive inotropy. This was concomitant with improved mitochondrial respiration (RCI 5.1 vs 9.3, P less than 0.01), higher tissue ATP content (10.3 vs 18.4 mumol/gdw P less than 0.01) and reduction of triglycerides (12.4 vs 8.0 mg/gww, P less than 0.01). These data suggest that propionyl-L-carnitine, when given chronically, is able to prevent erucic acid-induced cardiotoxicity, probably by reducing triglyceride accumulation and improving energy metabolism.

Adenosine Triphosphate↗
PubMed1991

Effect of propionyl-L-carnitine on mechanical function of isolated rabbit heart.

We studied the acute and chronic effects of propionyl-L-carnitine (PLC) on mechanical function of isolated rabbit heart. Propionyl-L-carnitine was either directly delivered in the perfusate (10(-9) to 10(-3) M) or intraperitoneally injected (250 mg/kg) for 10 days to the animals. When added acutely, propionyl-L-carnitine had no effect on inotropism, heart rate, or coronary perfusion pressure. When added chronically, propionyl-L-carnitine induced a positive inotropic effect, with no changes in heart rate or in coronary perfusion pressure, and it ameliorated the pressure-volume relationship. This effect of propionyl-L-carnitine was independent of the calcium concentration of the perfusion medium, but it was correlated with an increase in the myocardial content of propionyl-L-carnitine. The effect was not apparent after 5 days of treatment, although the tissue content of propionyl-L-carnitine remained unchanged. These data suggest that propionyl-L-carnitine, when given chronically, exerts a positive inotropic effect.

Acetylcarnitine↗
PubMed1991

Misleading results in studying pharmacodynamic interaction with oral anticoagulant.

We described an experimental condition, in which the i.p. administration of rats of irritants produces a misleading increase of the anticoagulant effect of warfarin. Group of 10 adult Wistar rats were treated i.p. or i.v. with HCl 0.1N plus warfarin p.o.; 24 hr after warfarin administration, prothrombin time was determined on citrate blood specimens and the animals were submitted to autopsy. When HCl is given i.p., a significant increase of prothrombin time is observed. On the contrary following i.v. administration no interference with the anticoagulant effect of warfarin is observed. Abdomen exploration of rats shows the presence of serum exudate following i.p. but not i.v. administration of HCl. The synergistic effect of i.p. administration of HCl on anticoagulant effect of warfarin appears an experimental artifact, probably attributable to a non-specific local irritating effect. This result stresses the need of caution in interpreting animal data indicating a synergism with oral anticoagulant.

Animals↗
PubMed1990

Misleading results in studying pharmacodynamic interaction with oral anticoagulants.

An experimental conditions is described in which the i.p. administration to rats of irritants produces a misleading increase of the anticoagulant effect of warfarin. Groups of 10 adult Wistar rats were treated i.p. or i.v. with HCl 0.1N plus warfarin p.o.; 24 hr after warfarin administration, prothrombin time was determined on citrate blood specimens and the animals were submitted to autopsy. When HCl is given i.p., a significant increase of prothrombin time is observed. On the contrary following i.v. administration no interference with the anticoagulant effect of warfarin is observed. Abdomen exploration of rats shows the presence of serum exudate following i.p. but not i.v. administration of HCl. The synergistic effect of i.p. administration of HCl on anticoagulant effect of warfarin appears an experimental artifact, probably attributable to a non-specific local irritating effect. This result stresses the need of caution in interpreting animal data indicating a synergism with oral anticoagulants.

Animals↗
PubMed1978

Comparative cardiovascular toxicity of trazodone and imipramine in the rat.

Several authors have associated the cardiotoxicity of the tricyclic antidepressants with their capacity to potentiate the response to catecholamines. Trazodone is a psychotropic drug with a clinically proven antidepressant activity. It differes from the tricyclic antidepressants under several aspects (chemistry, pharmacology, mode and mechanism of action, etc.), including interactions with catecholamines. Contrary to the tricyclic antidepressants, it does not potentiate the response to catecholamines, but, instead, has an adrenolytic activity. We therefore decided to compare the cardiotoxicity of trazodone and of a tricyclic antidepressant, i.e. imipramine in the rat. The experiments were conducted on anaesthetized Long Evans rats, the drugs being administered by i.v. infusion until cardiac arrest occurred; ECG (lead II) and blood pressure (BP) were recorded at the same time. The primary effect of trazodone was its hypotensive action. ECG changes, consisting of a lengthening of the PR interval, were observed only when there was a marked drop in BP. The primary effect of imipramine, instead, consisted of disturbances in cardiac conduction. It is concluded that trazodone and imipramine produce different cardiovascular effects.

Animals↗
PubMed1978

Acute cardiovascular toxicity of trazodone, etoperidone and imipramine in rats.

The cardiovascular effects of trazodone, a broad-spectrum antidepressant and its analogue etoperidone, were compared with imipramine, following intravenous infusion in rats. Their effects on electrocardiogram and blood pressure were simultaneously recorded until cardiac arrest. Hypotension was the primary effect of trazodone and etoperidone. ECG changes, i.e. lengthening of the PR interval, were observed only when the blood pressure reached very low values. On the other hand, imipramine produced first the well known ECG changes and then a drop in blood pressure. As far as mortality was concerned, trazodone was the least toxic drug, followed by etoperidone, whereas imipramine was most toxic; these differences being in agreement with the LD50 values reported in rats by the i.v. route. It is concluded that trazodone and etoperidone produce in rats cardiovascular effects, which are different from those of imipramine. Moreover these differences are consistent with their pharmacological properties, particularly their interaction with catecholamines, which are inhibited by trazodone or etoperidone and potentiated by imipramine.

Animals↗