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Biomedical subjects

R Lisciani

Publications and source records attributed to R Lisciani.

At least 19 recordsLinked to original sources
PubMed1999

Pharmacokinetics and acute tolerance of a double virus inactivated plasma derived factor VIII concentrate.

To further reduce the risk of possible viral disease transmission, an additional virucidal step was performed in the manufacturing process of a solvent/detergent treated factor VIII concentrate, which consisted of heating the lyophilized preparation at 100 degrees C for 30 min (Emoclot DI; ISI, Italy). Because thermal treatment may modify factor VIII bioavailability, the pharmacokinetic parameters and the acute tolerance of the single viral inactivated concentrate (preparation A) were compared with that of the double viral inactivated one (preparation B). Fifteen patients with severe haemophilia A and positive for HAV Ab were enrolled in a double-blind cross-over study and injected with 32.5 IU kg-1 of preparation A and 27 IU kg-1 of the preparation B. No significant differences between terminal half-life, area under the curve/dose, clearance/kg, volume of distribution at the steady state, in vivo recovery and acute tolerance of the two preparations was observed. The only statistical difference was restricted to Cmax.

Adolescent↗
PubMed1997

Myocardial fatty acid pattern in rats fed on an erucic acid enriched diet.

Individual lipid classes and their fatty acid pattern in myocardium of rats fed on a diet containing 10% erucic acid ethyl ester (cis-13-docosenoic acid ethyl ester) were investigated and compared to rats fed on a normal diet. Two groups of rats were treated for 10 consecutive days with the erucic acid ethyl ester diet and the standard diet, respectively. After extracting total lipids from the myocardium of the rats, the individual lipid classes and the percentage of fatty acids in phospholipids, free fatty acids, diglycerides and triglycerides were measured. The data obtained demonstrate that the erucic acid ethyl ester diet induces a marked increase in free fatty acids and in triglycerides and marked differences in fatty acid pattern in triglycerides, free fatty acids and diglycerides, but only marginal differences in phospholipids, which seem to be carefully preserved as fundamental components of cell and mitochondria membranes.

Animals↗
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↗
PubMed1986

Structure-analgesic activity relationships in a set of 2-aminobenzamide derivatives.

A set of 2-aminobenzamide derivatives designed as analgesic following the principles of correlation analysis have been prepared and tested. The analgesic effects shown by these products are similar to those of non-narcotic analgesic drugs; moreover, they do not show antipyretic effects and are inactive or very poor inhibitors of prostaglandin synthesis. Quantitative structure-activity relationships (QSAR) show that the analgesic potency (writhing test) is a function of the octanol-water partition coefficient. The predictive value of a correlation equation previously published is clearly demonstrated.

Acetaminophen↗
PubMed1984

Anti-inflammatory activity of Eryngium maritimum L. rhizome extracts in intact rats.

The administration of rough hydrophilic extract of Eryngium maritimum L. to intact rats inhibits carrageenin induced paw oedema, but it is inactive against cotton pellet granuloma; moreover, the extract does not reduce the weight of thymus, adrenals and spleen. These data show that the anti-inflammatory effect of E. maritimum extract is unlikely to be produced by a steroid-like compound or to be a consequence of adrenal stimulation. Further fractionation of total hydrophilic extract showed that the anti-inflammatory activity is retained by a sub-alkaline fraction.

Animals↗
PubMed1983

Possible dopaminergic involvement in biting compulsion induced by large doses of clonidine.

The effects of amphetamine, scopolamine, phenoxybenzamine, haloperidol and clozapine on biting compulsion induced by large doses of clonidine were studied in mice. Clonidine-induced biting compulsion was potentiated by amphetamine and scopolamine, and inhibited by phenoxybenzamine, haloperidol and clozapine. It appears that biting compulsion elicited by clonidine is mediated by the stimulation of both noradrenaline and dopamine in the brain. Since clorapine, an atypical neuroleptic agent, inhibits this response, the possibility is discussed to use clonidine-induced biting compulsion to detect neuroleptic agents devoid of extrapyramidal side effects.

Aggression↗
PubMed1982

Psychopharmacological profile of dapiprazole, a new potential antipsychotic agent.

3-[2-[4-(2-Methylphenyl)-1-piperazinyl]ethyl]-5,6,7,8-tetrahydro-1,2,4-triazolo[4,3-a]pyridine HCl (dapiprazole is a new compound endowed with a unique psychopharmacological profile. It inhibits amphetamine toxicity in grouped mice, and alcohol and morphine withdrawal syndromes, whereas it is almost inactive in the screening models for neuroleptics relying on dopaminergic activity. It also produces sedation, blocks conditioned avoidance reflex, reduces the response to noxious stimuli, has EEG synchronizing effects and inhibits the arousal reaction. Dapiprazole is a potent central and peripheral adrenolytic agent. Its acute toxicity is low. On the basis of these data, clinical investigations of dapiprazole are suggested in psychotic conditions such as the withdrawal syndromes, schizophrenia and schizo-affective disorders.

Animals↗
PubMed1982

General pharmacological properties of dapiprazole, a potential psychotropic agent.

A study of the general pharmacology of 3-[2-[4-(2-methylphenyl)-1-piperazinyl]ethyl]-5,6,7,8-tetrahydro-1,2,4-triazolo-[4,3-alpyridine HCl (dapiprazole), a new psychotropic agent, is reported. The predominant feature of this compound appears to be alpha-adrenergic blockade. This action has been observed both in vitro and in vivo. Dapiprazole also possesses antihistaminic and antiserotonin activities, although at relatively high doses. The antihistaminic action appears to be restricted to H1 receptors as suggested by the lack of activity on the guinea-pig atrium. Dapiprazole appears to be devoid of anticholinergic, local anaesthetic, antimicrobial and diuretic effects.

Anesthetics, Local↗
PubMed1982

Effects of dapiprazole on pupillary size and intraocular pressure in rabbits.

The effects of 3-[2-[4-(2-methylphenyl)-1- piperazinyl]ethyl]-5,6,7,8-tetrahydro-1,2,4-triazolo[4,3-a]pyridine HCl (dapiprazole), a new drug with alpha-adrenergic blocking properties, on pupillary diameter and intraocular pressure have been studied in rabbits. Following i.v. administration, a reduction of intraocular pressure is observed at doses devoid of activity on pupillary diameter. Following topical application, a miotic and ocular hypertensive action was observed at the same doses; the hypotensive action is produced in both normal rabbits and in rabbits with water load- or corticosteroid-induced ocular hypertension. Contact lenses increase the duration of effects of dapiprazole. These results suggest a potential interest of dapiprazole in glaucoma, with particular reference to the topical treatment of angle-closure glaucoma.

Administration, Topical↗
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↗