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PubMed1986

Forms of atypical depression and their response to antidepressant drugs.

Three definitions of atypical depression are evaluated with respect to the effects of monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs) on the basis of pooled data from several double-blind studies. Those three definitions of atypical depression are depression with associated panic, depression secondary to a diagnosis of anxiety, and depression with reversed vegetative change. In none of these forms was a drug difference observed. However, when gender was taken into account, MAOIs were superior to TCAs in depressed women with panic attacks, whereas TCAs were superior to MAOIs in depressed men with panic attacks.

Adult↗
PubMed1987

Studies of rhinovirus resistant to an antiviral chalcone.

During studies of the antiviral activity of chalcone Ro-09-0410 on human rhinovirus type 9 (RV9) chalcone-resistant strains of RV9 were isolated and appeared with a frequency of about 10(-5) in chalcone sensitive stock. Chalcone-dependent viruses were found after further passage. Some characteristics of the resistant viruses were studied and compared with those of the wild type virus; a number of differences were detected. They produced smaller plaques and grew to lower titre; they were no longer protected by chalcone from inactivation by heat and low pH. The event responsible for drug dependence apparently took place after that responsible for drug resistance. Drug-resistant viruses were still sensitive to dichloroflavan and enviroxime.

Antiviral Agents↗
PubMed1990

Comparative studies on the antirhinovirus activity and the mode of action of the rhinovirus capsid binding agents, chalcone amides.

Studies of various analogs related to the antirhinovirus agent 4'-ethoxy-2'-hydroxy-4,6'-dimethoxychalcone (Chalcone Ro 09-0410) led to the identification of amide analogs that are 4.5 to 10 times more active against human rhinovirus (HRV) in tissue culture as measured by chemotherapeutic indices. Chalcone amides Ro 09-0535, Ro 09-0696 and Ro 09-0881 inhibited viral replication at concentrations as low as less than 2-3 ng/ml and were cytotoxic between 30 to 50 micrograms/ml. These compounds bind to HRV and reduce the virus infectivity titers by 3 log10 or greater at 0.5 micrograms/ml for 60 min similar to Ro 09-0410. These amide analogs competitively inhibited the binding of [3H]Ro 09-0410 to the viral capsid similar to capsid binding antirhinovirus agents, Ro 09-0410, 4',6-dichloroflavan and WIN-51711. Furthermore, strains of HRV type 2 resistant to each of the above agents showed cross-resistance to all other agents. These results indicate that the chalcone amides also bind to the same or close-proximity site for the capsid binding antirhinovirus agents, which is on the specific site within the viral capsid protein. However, differences in the degree of the inhibition of [3H]Ro 09-0410 binding, cross-resistance of strains of HRV resistant to the agents and HRV serotype specificity were observed not only between the chalcone amides and the other antivirus agents (Ro 09-0410, 4',6-dichloroflavan and WIN-51711) but also among the chalcone amides, particularly between Ro 09-0535 and Ro 09-0696. These differences are presumably due to alterations in the binding affinities of compounds as a consequence of variations in the shape and size of the hydrophobic pocket that exists between serotypes including resistant strains.

Amides↗
PubMed1985

A method for evaluating different modes of action of an antiarrhythmic drug in man. The effects of propafenone on sinus nodal functions.

In vitro experiments have shown that the antiarrhythmic effects of propafenone are due to a direct depressant action and to a beta-blocking activity. In this study a method was used to evaluate the direct effect and the autonomically mediated actions of an antiarrhythmic agent in a clinical setting. An electrophysiological study was performed twice, at an interval of 24 hr, in 17 patients (age: 52 +/- 17 years) with normal resting and intrinsic heart rate. In the first study the overall effect of intravenous propafenone (1.5-2 mg/kg) was evaluated by comparing the sinus node parameters obtained during the basal state and after drug administration. In the second study the direct depressant effect of the drug was evaluated by comparing the electrophysiological variables obtained following autonomic blockade (propranolol 0.2 mg/kg and atropine 0.04 mg/kg) and after propafenone. In the first study there was no significant change in the sinus cycle length and corrected sinus node recovery time and only a small (9.1%) increase in sinuatrial conduction time, whereas in the second study these variables increased significantly. The degree of increase in sinus cycle length and corrected sinus node recovery time was significantly higher in the second study than in the first one. These data suggest that: (1) propafenone has direct depressant effect on sinus automaticity but this effect is counteracted by autonomically mediated actions (most likely of vagolytic type); (2) the beta-blocking effect of the drug demonstrated in isolated atria is not seen in a clinical setting.

Adolescent↗
PubMed1985

Lidocaine, mexiletine and propafenone in the treatment of arrhythmias complicating myocardial infarction. A case report.

We describe a case of acute myocardial infarction complicated by atrial and ventricular arrhythmias in which it was possible to verify the effectiveness of lidocaine, mexiletine and propafenone. Intravenous administration of mexiletine was ineffective both on atrial and ventricular rhythm disturbances. The lidocaine therapy reduced ventricular ectopic frequency, but did not prevent the appearance of several paroxysms of atrial fibrillation. Intravenous infusion of propafenone, 11 micrograms/kg per min, after a 1 mg/kg i.v. bolus, immediately and completely suppressed atrial arrhythmias. The increase in infusion rate up to 22 micrograms/kg per min also suppressed ventricular ectopy. This dosage of propafenone did not provoke serious adverse effects in our patient.

Anti-Arrhythmia Agents↗
PubMed1991

Topical photoprotection for hereditary polymorphic light eruption of American Indians.

We evaluated the photoprotective efficacy of a broad-spectrum sunscreen containing a UVA screen (butyl methoxydibenzoylmethane) and a UVB screen (octyl dimethyl p-aminobenzoic acid) in patients with hereditary polymorphic light eruption. At least 18 of the 30 patients who enrolled in the study were sensitive to sunlight through window glass, an indication of UVA sensitivity. Of the 21 patients who completed the clinical trial, the physician's evaluation was that 18 (86%) obtained good to excellent results. Self-evaluation by the patients revealed that 16 (76%) noted more photoprotection than from previous treatments.

4-Aminobenzoic Acid↗
PubMed1992

Topical anesthetic-induced methemoglobinemia in sheep: a comparison of benzocaine and lidocaine.

Benzocaine induces methemoglobin (MHb) in several species, whereas lidocaine may increase MHb in cats and human. Elevated MHb (greater than 20%) in sheep after benzocaine exposure was recently recognized. MHb decreases blood oxygen-carrying capacity which can complicate interpretation of experimental data. Sheep are used in research which requires tracheal intubation and blood gas analysis. Since benzocaine and lidocaine are used to provide local anesthesia prior to intubation, we compared MHb production by sheep after exposure to these drugs. A dose-response relationship between benzocaine and MHb was investigated. Eight crossbred Dorset ewes were dosed intranasally with benzocaine for 2 sec or with 40 mg of lidocaine in a randomized crossover design. Sheep with elevated MHb after the 2-sec benzocaine dose were later dosed with benzocaine intranasally for 10 sec. MHb levels were measured periodically on a CO-Oximeter. A quantitative MHb response to an indirect MHb former, p-aminopropiophenone (PAPP), by each sheep was determined 15 min after PAPP (0.6 mg/kg iv). MHb levels remained at baseline (1-2%) after lidocaine exposure in all sheep, as well as in four sheep (nonresponders) after the 2-sec benzocaine dose. Four sheep (responders) demonstrated 16.5-26.4% MHb after the 2-sec benzocaine dose. The responders formed 38.2-50.5% MHb after the 10-sec benzocaine dose. All responders developed high MHb after PAPP, while nonresponders developed slightly elevated MHb after PAPP. An N-hydroxy metabolite of benzocaine is the likely active MHb-forming substance. Benzocaine should be replaced by lidocaine when local anesthesia of the nasal or oropharyngeal region in sheep is required.

Administration, Topical↗
PubMed1984

Evaluating drug effects on children's cognitive functioning.

In our studies of drug therapy in child psychiatry disorders, we have been using a battery of tests to monitor any effects of medication on the various components of cognitive processing. Our intention was to measure skills required by the children for successful classroom performance. We have used this test battery approach in open clinical trials of bupropion (Wellbutrin) and of alprazolam (Xanax) with child psychiatry patients. On no single test was the effect of bupropion vs placebo significant; however, there was no indication of any cognitive deterioration with bupropion. Group performance with alprazolam was more variable, and again no individual test showed significant changes with medication. These initial applications of the cognitive battery indicate that bupropion, a new antidepressant and alprazolam, an anxiolytic have no adverse effects on cognition at therapeutically effective doses.

Alprazolam↗
PubMed1985

Dopamine uptake blockers protect against the dopamine depleting effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse striatum.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a recently described neurotoxin, produces a marked dopamine (DA) depletion in the mouse striatum. In this study, a series of DA uptake blockers was tested for their ability to prevent this effect of MPTP. The agents tested (amfonelic acid, benztropine, bupropion and mazindol) completely protected against DA depletion in the mouse striatum when given before DA-depleting doses of MPTP were administered, whereas atropine and trihexyphenidyl (which were employed for comparative purposes) did not. DA uptake blocking agents appear to represent a second general class of compounds, monoamine oxidase inhibitors being the first, which protect against the biologic effects of MPTP in the mouse.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1990

Effects of Eperisone on Renshaw cells of cats.

Actions of Eperisone (4'-ethyl-2-methyl-3-piperidinopropiophenone; EMPP) on Renshaw cells were investigated on spinal cats. The characteristic high-frequency discharges of Renshaw cells within 20 ms following antidromic ventral root stimulation were depressed while the later responses which follow the earlier responses for 80 ms were enhanced following administration of EMPP. These effects suggest that EMPP has differential effects on nicotinic acetylcholine receptors of the Renshaw cells.

Action Potentials↗
PubMed1992

Antinociceptive effects of tizanidine, diazepam and eperisone in isolated spinal cord-tail preparations of newborn rat.

Antinociceptive effects of three centrally acting muscle relaxants, tizanidine, diazepam and eperisone, were studied using an isolated newborn rat spinal cord-tail preparation. Potentials were recorded from a lumbar ventral root (L3-L5) extracellularly using a suction electrode. Pinch stimulation applied to the tail elicited a depolarizing response in the ventral root lasting 15-30 sec, referred to as the tail-pinch potential. Electrical stimulation of the ipsilateral dorsal root of the same segment with a single shock induced depolarizing responses in the ventral root. The responses consisted of monosynaptic and polysynaptic reflexes with a fast time course, followed by a slow depolarizing response lasting about 20 sec. The latter slow response was designated the ipsilateral slow ventral root potential (VRP). Both the tail-pinch potential and the ipsilateral slow VRP were depressed by application to the spinal cord of tizanidine (2-3 microM), diazepam (2 microM) and eperisone (100-200 microM). The effect of tizanidine was reversed by alpha 2-adrenoreceptor antagonists, yohimbine and idazoxan, but not by an alpha 1-antagonist, prazosin. The effect of diazepam was reversed by the benzodiazepine antagonist, flumazenil.

Analgesics↗
PubMed1983

Alkyl chain length and acute oral toxicity of p-aminophenones.

There exists a structure-toxicity relationship between the length of the alkyl chain of p-aminopropiophenone homologues and their oral LD50's in albino mice and rats. The acute oral toxicity decreased in both species with the removal of one carbon atom from the alkyl group, increased with the addition of one and two carbon atoms, and decreased again with the addition of three carbon atoms to the alkyl group.

Administration, Oral↗
PubMed1986

Bupropion. Effects on cerebral monoamines in rat and on blood pressure in dog.

Intravenous injections of bupropion into the femoral vein of dogs did not change cardiovascular peripheric responses because it did not affect significantly either arterial pressure or heart rate. In acute experiments bupropion increased the levels of DA, NA and 5-HT in the brain of rats. There was a remarkable correlation between the levels of monoamines and the hypermotility.

4-Aminobutyrate Transaminase↗