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At least 703 records · Page 39Linked to original sources
PubMed1997

Methcathinone intoxication in the rat: abrogation by dextrorphan.

STUDY OBJECTIVE: Methcathinone, a designer drug, has high abuse liability. In this study we characterized acute methcathinone toxicity in rats, attempting to determine whether the excitatory amino acid receptor antagonist dextrorphan can antagonize methcathinone intoxication. METHODS: Intoxication was produced with IV methcathinone infusion (5 mg/kg/minute; 100 mg/mL) in conscious rats. We studied pretreatment, in which dextrorphan or vehicle was injected 30 minutes before methcathinone infusion. In a second protocol, dextrorphan or saline solution was given immediately after the onset of convulsions. RESULTS: Methcathinone caused tachycardia (maximal increase, 131 +/- 10 beats/minute), hyperthermia (+2.3 degrees C), convulsions, and cardiorespiratory collapse in vehicle-pretreated rats (n = 9). Death occurred after 32.0 +/- 1.1 minutes of infusion. Dextrorphan pretreatment (25 mg/kg; n = 7) significantly reduced hyperthermia (+.1 degree +/- .3 degree C) and tachycardia and increased the convulsive (dextrorphan, 134 +/- 9 mg/kg; vehicle, 67 +/- 4 mg/kg) and lethal doses (dextrorphan, 204 +/- 9 mg/kg; vehicle, 160 +/- 5 mg/kg). Dextrorphan, given immediately after the initial methcathinone convulsion, reduced hyperthermic and tachycardic responses but not the lethality of methcathinone. CONCLUSION: Blockade of excitatory amino acid receptors by dextrorphan minimizes acute methcathinone intoxication.

Animals↗
PubMed1982

A comparison of the safety and efficacy of bupropion HCL and amitriptyline hcl in depressed outpatients.

1. Thirty adult outpatients diagnosed with depressive illness were treated with either bupropion HCL or amitriptyline HCL. 2. Weekly ratings of efficacy and safety were undertaken using the Hamilton Depression, Hamilton Anxiety, Clinical Global Improvement, and Treatment Emergent Symptom Scales. Periodic physical investigations were also performed. 3. After 4 weeks of active treatment patients in both drug groups showed significant improvement on all rating scales. 4. The side effect profile of each drug was clinically different from one another with a notable absence of anticholinergic side effects characteristic of the bupropion group. 5. No significant laboratory or physical changes were found although slight changes in weight were noted with bupropion patients having a slight weight loss and amitriptyline patients a slight weight gain. There were no withdrawal effects from discontinuing either drug.

Adult↗
PubMed2001

Influence of prenylated and non-prenylated flavonoids on liver microsomal lipid peroxidation and oxidative injury in rat hepatocytes.

Prenylated chalcones from hops and beer were compared with non-prenylated flavonoids [chalconaringenin (CN), naringenin (NG), genistein (GS) and quercetin (QC)] for their ability to inhibit lipid peroxidation in rat liver microsomes. Chalcones with prenyl- or geranyl-groups (5 and 25 microM) were more effective inhibitors of microsomal lipid peroxidation than CN, NG or GS induced by Fe(2+)/ascorbate. Prenylated chalcones were effective inhibitors of microsomal lipid peroxidation induced by Fe(3+)-ADP/NADPH and by tert-butyl hydroperoxide (TBH) but to a lesser extent compared to the Fe(2+)/ascorbate system. An increase of prenyl substituents decreased antioxidant activity in the lipid peroxidation systems. Certain flavonoids behaved as prooxidants in the iron-dependent lipid peroxidation systems. For example, at 5 microM, NG enhanced iron/ascorbate-induced lipid peroxidation whereas CN, diprenylxanthohumol and tetrahydroxanthohumol enhanced Fe(3+)-ADP/NADPH-induced lipid peroxidation. None of the flavonoids (25 microM), except QC, inhibited NADPH cytochrome P450-reductase activity of rat liver microsomes, suggesting that the mechanism of inhibition of lipid peroxidation induced by Fe(3+)-ADP/NADPH is not due to inhibition of the reductase enzyme. Chalcones exhibiting antioxidant activity against TBH-induced lipid peroxidation such as xanthohumol and 5'-prenylxanthohumol, and NG, with no antioxidant property at 5 microM concentration protected cultured rat hepatocytes from TBH toxicity. Other antioxidants (desmethylxanthohumol and CN) in the TBH system were not cytoprotective. These results demonstrate the importance of prenyl groups in the antioxidant activity of hop chalcones in the various in vitro systems of lipid peroxidation. Furthermore, the antioxidant activity of the flavonoids has little or no bearing on their ability to protect rat hepatocytes from the toxic effects of TBH.

Animals↗
PubMed2001

Identification, quantitation and biological activity of phytoestrogens in a dietary supplement for breast enhancement.

A hop-based dietary supplement, marketed for natural breast enhancement, was analysed to determine the identity and biological activity of active constituents and potential biological effects in man. Extracts of the dietary supplement were analysed by LC-MS(n) and phytoestrogens identified and quantitated by reference to appropriate standards. Only hop-associated phytoestrogens were found in the dietary supplement at significant concentrations as follows (mean+/-1 S.D.); 8-prenylnaringenin 10.9+/-0.3, 6-prenylnaringenin 27.4+/-1.2, 6,8-diprenylnaringenin 0.9+/-0.1, xanthohumol 321+/-17 and isoxanthohumol 81.1+/-1.6 microg/g of dietary supplement. The oestrogenic activity of extracts in an ERalpha reporter gene assay was equivalent to 48+/-6.3 ng 17beta-oestradiol/g supplement and consistent with the 8-prenylnaringenin content. The dietary supplement extract also inhibited reductive 17beta-hydroxysteroid oxidoreductase activity, but to a greater extent than a concentration matched reference mixture of hop phytoestrogens. However, the supplement was only weakly active in mouse uterotrophic assays following administration in feed or after subcutaneous injection of extract at doses of 8-PN up to 250 times higher than that recommended for women. These preliminary findings suggest that the dietary supplement is unlikely to produce oestrogenic effects in vivo at the level of the uterus; supporting evidence is still required to demonstrate efficacy.

Animals↗
PubMed1997

Extraneuronal uptake inhibitor U-0521 decreases contractile responses in rat vas deferens.

1. The influence of catechol-O-methyltransferase inhibitor U-0521 on isotonic contraction of isolated rat vas deferens was examined to determine optimal concentration and nonspecific effects. 2. Maximum responses to (-)-epinephrine were increased at 0.4 microM and 1 microM concentrations of U-0521. Epinephrine responses were progressively decreased in the presence of higher concentrations (10 microM, 30 microM and 100 microM) of U-0521. 3. The response to the nonadrenergic agonist neurokinin A was similarly depressed in the presence of 100 microM U-0521. 4. U-0521 not only inhibits COMT, at concentrations above 1 microM it nonspecifically depresses contraction of the rat vas deferens by both adrenergic and nonadrenergic agonists.

Adrenergic alpha-Agonists↗
PubMed1999

Pharmacological effects of methamphetamine and other stimulants via inhalation exposure.

The effects of methamphetamine-HCl, methcathinone-HCl, cocaine and ephedrine on locomotor stimulation were compared between inhalation exposure and i.v. injection in mice. Methamphetamine-HCl was readily volatilized upon heating at 300 degrees C in a glass pipe with only trace amounts of amphetamine being produced. The ED50 dose (9.4 and 6.5 mumol/kg for inhalation exposure and i.v. injections, respectively) and biodisposition of methamphetamine-HCl were similar for both routes of administration. Methcathinone-HCl and cocaine were readily volatilized. Their dose response profiles also appeared similar for both routes of administration. Ephedrine did not appear to be easily volatilized and was only effective in stimulating locomotor activity after i.v. administration. These findings indicate that inhalation exposure to methamphetamine-HCl, cocaine and methcathinone possess similar pharmacological characteristics as the i.v. route of administration. In particular, this model may have implications in predicting the pharmacological activity of various stimulants via the inhalation route of administration.

Administration, Inhalation↗
PubMed1985

Determination of plasma protein binding of propafenone in rats, dogs and humans by highly sensitive gas chromatography-mass spectrometry.

A highly sensitive method for the determination of propafenone in plasma has been established using gas chromatography-mass spectrometry with the deuterium-labelled compound as an internal standard. Plasma levels as low as 1 ng/ml were measured using 0.5-ml plasma samples. Plasma protein binding of the drug in rats, dogs and humans in vitro and in vivo was determined by the proposed method. About 90% of the drug was bound to the plasma protein in all species in vitro (20-500 ng/ml) and 69-88% in rats, 90-95% in dogs and 77-89% in humans after oral administration of the drug at doses of 50 mg/kg, 5 mg/kg and 200 mg per person, respectively.

Adrenergic beta-Antagonists↗
PubMed2003

Optimization of a simple method for the chiral separation of methamphetamine and related compounds in clandestine tablets and urine samples by beta-cyclodextrine modified capillary electrophoresis: a complementary method to GC-MS.

The chiral separation of (+/-)-methamphetamine, (+/-)-methcathinone, (+/-)-ephedrine and (+/-)-pseudoephedrine by means of beta-cyclodextrine modified capillary electrophoresis is described. The distribution of enantiomers in clandestine tablets and urine samples were identified. Several electrophoretic parameters such as the concentration of beta-cyclodextrin, temperature, the applied voltage and the amount of organic solvent required for successful separation were optimized. The method, as described herein, represents a good complementary method to GC-MS for use in forensic and clinical analysis.

Central Nervous System Stimulants↗
PubMed1984

Electrophysiologic and hemodynamic effects of intravenous propafenone in patients with recurrent ventricular tachycardia.

Electrophysiologic and hemodynamic studies were performed before and after intravenous infusion of a new antiarrhythmic agent, propafenone, in 28 patients with recurrent ventricular tachycardia. Propafenone was given at a loading dose of 2 mg/kg in all patients. Subsequently, group A, the first 14 patients, received 1 mg/min and group B, the second 14 patients, received 2 mg/min continuous infusion. Propafenone exerted no effect on sinus nodal recovery time and sinoatrial conduction time, but significantly prolonged atrioventricular (AV) nodal and His-Purkinje conduction time and the QRS duration (respectively, 95 +/- 19, 48 +/- 10 and 120 +/- 23 ms before, and 110 +/- 28, 53 +/- 10 and 135 +/- 27 ms after; p less than 0.001). Propafenone did not change the mean arterial blood pressure but slightly increased right atrial, pulmonary artery and capillary wedge pressures resulting in mild depression of the cardiac index (2.6 +/- 0.8 liters/min per m2 before and 2.3 +/- 0.7 liters/min per m2 after; p less than 0.001). None of the patients were symptomatic from these changes. In group A, propafenone did not affect the inducibility of ventricular tachycardia except for one patient whose arrhythmia was sustained before and become nonsustained after propafenone. In group B, sustained ventricular tachycardia became noninducible in three patients and nonsustained in two patients, and nonsustained ventricular tachycardia became noninducible in one patient after propafenone. Therefore, an appropriate loading dose of intravenous propafenone such as 2 mg/kg followed by 2 mg/min infusion may be given safely and may suppress ventricular tachycardia. Propafenone may be a useful addition to currently available antiarrhythmic agents.

Adolescent↗
PubMed1984

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

Anti-Arrhythmia Agents↗
PubMed1984

Propafenone: a new agent for ventricular arrhythmia.

Propafenone, a new antiarrhythmic agent, was utilized in 30 patients with diverse heart disease who presented with sustained hemodynamically unstable ventricular arrhythmia. Drug efficacy was judged by means of ambulatory electrocardiographic monitoring and exercise testing. Nine patients additionally had invasive electrophysiologic studies. Seventeen patients (57%) responded to therapy as judged by monitoring and 21 patients (70%) responded to therapy as judged by exercise testing. When both methods were considered, 16 patients (53%) responded. The acute drug test predicted the result of maintenance therapy in 91% of patients. Seven of nine patients who had electrophysiologic testing responded based on this technique, and in all cases the results were concordant with the noninvasive evaluation. Serum blood levels did not correlate with antiarrhythmic effect. In patients with myocardial impairment, echocardiographic assessment of left ventricular function indicated a decrease in ejection fraction during propafenone therapy (32 versus 24%, p less than 0.05), while no change was observed in patients with normal left ventricular function. Side effects occurred in nine patients and included exacerbation of congestive heart failure, development of conduction abnormalities and aggravation of arrhythmia, each occurring in two patients. Ten patients who continued on long-term propafenone therapy for an average of 10 months (range 3 to 13) have remained free of arrhythmia and side effects. Propafenone needs to be employed with caution in patients with congestive heart failure or evidence of conduction system disease.

Adolescent↗
PubMed1985

Electrophysiologic effects and clinical efficacy of oral propafenone therapy in patients with ventricular tachycardia.

The effects of the antiarrhythmic agent propafenone were evaluated in 25 patients with recurrent symptomatic ventricular tachycardia. Oral propafenone was given to a maximal dose of 300 mg every 8 hours. Ten of the 25 patients developed side effects or had inadequate suppression of spontaneous ventricular arrhythmias during propafenone therapy. Electrophysiologic studies were performed before and during drug therapy on the 15 patients who had a satisfactory clinical response. Propafenone increased the PR interval from 168 +/- 46 to 188 +/- 25 ms (p less than 0.007), the HV interval from 47 +/- 10 to 65 +/- 13 ms (p less than 0.005), the shortest atrial pacing cycle length to maintain 1:1 atrioventricular (AV) nodal conduction from 385 +/- 44 to 436 +/- 42 ms (p less than 0.005), the ventricular effective refractory period from 231 +/- 17 to 255 +/- 19 ms (p less than 0.001) and the ventricular functional refractory period from 260 +/- 15 to 278 +/- 17 ms (p less than 0.002). Before propafenone therapy, all 15 patients had ventricular tachycardia induced by programmed ventricular stimulation. During propafenone treatment, 12 patients still had ventricular tachycardia induced, and the tachycardia cycle length significantly increased from 236 +/- 44 to 374 +/- 103 ms (p less than 0.001). Ten patients were considered to have satisfactory electrophysiologic response to propafenone on the basis of either the inability to initiate ventricular tachycardia or a marked increase in ventricular tachycardia cycle length associated with lack of symptoms during the induced tachycardia. These patients were discharged receiving propafenone.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed2002

The effects of derivatives of the nitroxide tempol on UVA-mediated in vitro lipid and protein oxidation.

Derivatives of tetramethylpiperidines are extensively employed in polymers to prevent photooxidation, and their stabilizing effect is attributed to the activity of the nitroxide radical derived from the parent amine. In this study, we examined the photoprotective effect of a commercial polymer photostabilizer, HALS-1, its corresponding nitroxide, bis(2,2,6,6-tetramethyl-piperidine-1-oxyl-4-yl)sebacate (TINO), and two derivatives of the piperidine nitroxide TEMPOL, 2,2,6,6-tetramethyl-piperidin-4-acetyloxy-1-oxyl (TEMP2) and 2,2,6,6-tetramethyl-piperidin-4-octanoyloxy-1-oxyl (TEMP8) synthesized by us, in liposomes exposed to ultraviolet A (UVA) radiation. For comparison, the UVA-absorber, 4-tert-butyl-4'-methoxydibenzoylmethane (Parsol 1789) used in many suncream formulations, was also included. The nitroxide TINO resulted extremely efficient at inhibiting aldehydic breakdown products deriving from 30 min exposure of liposomes to UVA and the protection was dose-dependent (10-100 microM). The corresponding amine HALS-1 was the least efficient while protection increased in the order: TEMP2 < Parsol 1789 < TEMP 8. HALS-1, TINO, and the two TEMPOL derivatives were also tested in a simple protein system consisting of bovine serum albumin (BSA) exposed to UVA. In this case, these compounds did not inhibit nor enhance UVA-mediated protein carbonyl formation in BSA. The differences in protection between the compounds are discussed in relation to their chemical reactivity, UVA-absorbing capacities, and their molecular structure. Overall, the results obtained envisage the potential use of nitroxide compounds as topical antioxidants.

Animals↗