Drugs online research references
J Auton Nerv Syst. 1990 Jun;30(2):175-7.
The pupil response to E-10-hydroxynortriptyline in rabbits with ocular sympathetic paresis.
Mindel JS, Rubin MA, Kharlamb AB.
Mount Sinai School of Medicine, Department of Ophthalmology, New York, NY 10029.
E-10-hydroxynortriptyline, a metabolite of nortriptyline with half the norepinephrine re-uptake blocking potency of the parent drug, but only 5% of its anticholinergic effect, was as effective as cocaine in demonstrating ocular sympathetic paresis. In five rabbits with unilateral superior cervical ganglionectomies, bilateral 5% cocaine HCl or E-10-hydroxynortriptyline maleate eye drops increased (P less than 0.001) the mean +/- SE anisocoria at 1 h by 1.84 +/- 0.03 mm or 2.16 +/- 0.33 mm, respectively. A single drop of E-10-hydroxynortriptyline did not alter corneal thickness or endothelial cell count.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2370421&dopt=Abstract
Psychopharmacology (Berl). 1985;87(2):212-5.
Cardiovascular effects of amitriptyline in the treatment of elderly depressed patients.
Christensen P, Thomsen HY, Pedersen OL, Thayssen P, Oxhoj H, Kragh-Sorensen P, Gram LF.
Thirteen elderly depressed patients (age 60-82 years) were treated for 5 weeks with a fixed dose of amitriptyline 100 mg (sustained release preparation). In all patients the sum of concentrations of amitriptyline and nortriptyline exceeded 130 micrograms/l, which is the recommended plasma level. Cardiovascular side effects were recorded by monitoring heart rate, blood pressure, standard ECG and systolic time intervals. During treatment, a transient increase in the supine heart rate was observed without significant changes in the supine blood pressure. The orthostatic drop in blood pressure was markedly increased during treatment without a compensatory increase in heart rate, and these changes remained significant during the whole investigational period. PQ and QRS were significantly increased during treatment, and significant changes in the systolic time intervals were found indicating impairment of myocardial conduction and contractility. In three patients medication was discontinued due to cardiovascular side effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3931149&dopt=Abstract
Exp Parasitol. 1984 Oct;58(2):194-208.
Fasciola hepatica: the effects of neuropharmacological agents upon in vitro motility.
Holmes SD, Fairweather I.
The effects of a wide range of neuropharmacological agents on the motility in vitro of Fasciola hepatica have been determined using an isometric transducer system. The neuromuscular blocking agents tubocurarine and decamethonium cause a long-term stimulation of the basal activity of the fluke. Acetylcholine causes an inhibition of activity. This effect is mimicked by the cholinergic agonists carbachol and nicotine, antagonised by the cholinergic blocking agents atropine and mecamylamine, and potentiated by eserine, a cholinesterase inhibitor. With nicotine and atropine the effects are accompanied by an increase in muscle tone at a concentration of 1 X 10(-2) M. Noradrenaline and adrenaline also cause some inhibition of activity, an effect antagonised by guanethidine, which blocks the release of noradrenaline. In contrast, dopamine stimulates fluke motility, whilst its antagonist dihydroergotamine causes an inhibition of activity. The monoamine oxidase inhibitors iproniazid and p-chloromercuribenzoic acid induce a stimulation of activity; with the latter there is an increase in muscle tone at a concentration of 1 X 10(-3) M. The amine depleting agents chloroamphetamine and reserpine, and the monoamine uptake inhibitors desipramine and nortriptyline produce an inhibition of fluke activity, as does the serotonin uptake inhibitor fluoxetine. High concentrations of chloroamphetamine (1 X 10(-2) M) and the uptake inhibitors (1 X 10(-3) M and above) also induce an increase in muscle tone. Serotonin causes a marked stimulation of motility. The pharmacological evidence is consistent with a neurotransmitter role of acetylcholine (inhibitory), dopamine (excitatory), and noradrenaline (inhibitory). The status of serotonin is discussed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6148259&dopt=Abstract
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