Drugs online research references
Biol Psychiatry. 1982 May;17(5):535-46.
Nortriptyline and EEG sleep in depressed patients.
Kupfer DJ, Spiker DG, Rossi A, Coble PA, Shaw D, Ulrich R.
The effect of nortriptyline was assessed on the EEG sleep of 20 inpatients with major depressive syndrome. While 25 mg of nortriptyline had an immediate effect on REM sleep variables, relatively little influence on sleep continuity measures was noted. Subsequent administration of 75 and 100 mg of nortriptyline produced continued REM sleep suppression over several weeks. In summary, nortriptyline altered EEG sleep in a pattern similar to that of amitriptyline. REM latency and REM sleep time were consistently reduced by drug administration, while REM activity was only transiently altered as with amitriptyline. The comparison with amitriptyline showed, for the most part, similar influences on REM sleep without the sedative effects of amitriptyline.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7093390&dopt=Abstract
Clin Pharmacol Ther. 1980 Jul;28(1):121-9.
Interindividual differences in amitriptyline demethylation.
Rollins DE, Alvan G, Bertilsson L, Gillette JR, Mellstrom B, Sjoqvist F, Traskman L.
Amitriptyline (AT) and its demethyl metabolite nortriptyline (NT) were given orally and intramuscularly to 6 normal subjects, and the areas under the blood concentration--time curves (AUC) were calculated. The mean unbound fraction of AT and NT in plasma was 5.4% and 8.3%, respectively. The blood-plasma ratio of NT was nearly double that of AT, which was close to unity. The mean systemic availability of oral relative to intramuscular AT and NT was 43% and 61%. The calculated mean oral blood clearance of AT as measured by dose (oral)/AUC was 1.6 1/min. The demethylation of orally administered AT varied considerably between the 6 individuals (from 25% to 89%) and correlated with oral drug clearance. Demethylation was estimated from the AUC applied to the NT metabolite. The estimated oral clearance of AT from demethylation ranged from 0.21 to 1.80 1/min.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7389249&dopt=Abstract
J Toxicol Clin Toxicol. 1988;26(3-4):223-32.
Clonidine interaction in amitriptyline poisoning.
Knudsen K, Ricksten SE, Heath A.
Department of Anesthesia and Intensive Care, University of Gothenburg, Sahlgren's Hospital, Sweden.
The effect of clonidine on amitriptyline-induced cardiotoxicity was investigated in an experimental rat mode. A continuous infusion of amitriptyline (30 mg/kg/h) was given until the animal died, usually within 2 hours. Fifteen minutes after starting the amitriptyline infusion, 50 micrograms/kg of clonidine was given intravenously over five minutes. This led to an increase in blood pressure and left ventricular end-diastolic pressure. There was no significant change in cardiac contractility. Heart rate decreased. These changes can be explained by an increase in afterload due to peripheral vasoconstriction. No signs of reduced sympathetic outflow were seen on the ECG. The peripheral effects of clonidine dominated over the central effects, which may be due to a competitive inhibition of amitriptyline at central noradrenergic sites. An increased afterload pushes the heart towards failure and increases mortality. In this model, clonidine did not reverse amitriptyline-induced cardiovascular toxicity. It may even be potentially harmful if used to treat tricyclic antidepressant poisoning.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3418777&dopt=Abstract
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