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At least 19 recordsLinked to original sources
PubMed1975

Cardiovascular effects of amitriptyline, nortriptyline, protriptyline, and doxepin in conscious rabbits after subacute pretreatment with protriptyline.

Conscious rabbits which had been permanently catheterized into their aortas and posterior caval veins, were injected daily with 10 mg/kg of protriptyline subcutaneously, divided in 3 doses. The blockade of the membrane pump in sympathetic nerve terminals by protriptyline was checked by pressor tests with noradrenaline (NA) and tyramine. In the presence of the membrane pump blockade 2.5 mg/kg of amitriptyline, nortriptyline, or protriptyline, or 3.0 mg/kg of doxepin was injected i.v. The antidepressants lowered blood pressure transiently and increased the heart rate, doxepin and amitriptyline being more effective than nortriptyline and protriptyline. Amitriptyline and doxepin provoked more severe cardiac arrhythmias on ECG than nortriptyline, and protriptyline caused no arrhythmias. Intravenous infusion of NA (11 mug/min) raised the blood pressure and lowered the heart rate. Injection of antidepressants during NA infusion resulted in more pronounced depressor and tachycardic effects than occurred without NA infusion. Major ECG changes were only slightly more apparent than without NA infusion. The rank order of toxicity of the antidepressants was the same. It is concluded that the NA potentiation by tricyclic antidepressants is not the main reason for their cardiotoxic effects.

Amitriptyline↗
PubMed1993

[Effects of protriptyline on day and night time oxygenation in patients with chronic obstructive pulmonary disease].

To determine the effects of protriptyline, a tricyclic non-sedative antidepressant, on sleep architecture, day and night arterial oxygen saturation and pulmonary function, ten patients with stable chronic obstructive pulmonary disease were evaluated. Overnight polysomnographic measurements were made before and 2 to 4 months after Protriptyline (10-20 mg daily) therapy. The results showed that two patients could not tolerate the protriptyline. Protriptyline caused xerostomia in eight of 10 cases, dysuria in five of 10 cases. Protriptyline therapy did not alter sleep efficiency and sleep latency but shortened the REM sleep stage from 15.6% to 8.2% Even though protriptyline did not change simple spirometry comparing before and after therapy, protriptyline decreased delta SaO2 and increased lowest SaO2 and baseline PaO2. In conclusion, these results suggest that protriptyline may benefit COPD patients by improving nocturnal oxygenation and nocturnal desaturation events.

Aged↗
PubMed1978

Protriptyline kinetics.

The kinetics of protriptyline were examined in 8 subjects after a single oral dose of 30 mg protriptyline hydrochloride. Peak protriptyline levels ranged from 10.4 to 22.3 ng/ml and were reached 6 to 12 hr after the oral dose. The mean protriptyline half-life (t1/2) was 74.3 hr and ranged from 53.6 to 91.7 hr in individual subjects, confirming the long t1/2 of protriptyline reported by Moody and associates. The estimated first-pass metabolism of protriptyline was relatively small, ranging from 10% to 25% of the oral dose, assuming complete absorption. The mean volume of distribution was 22.5 L/kg and ranged from 15.0 to 31.2 L/kg. No relationship was found between the kinetics of protriptyline and those of doxepin studied previously in 7 of the 8 subjects.

Adult↗
PubMed1993

Long-term effects of protriptyline in patients with chronic obstructive pulmonary disease.

Protriptyline has been shown to improve nocturnal and diurnal hypoxemia in patients with chronic obstructive pulmonary disease in short trials. We prospectively evaluated the long-term effects of protriptyline on pulmonary functions (lung volume and expiratory flow, arterial blood gases) and sleep characteristics (sleep architecture, nocturnal desaturations) in these patients. Sixteen patients previously studied before and after 10 wk of protriptyline treatment were reevaluated after a long-term follow-up (range, 18 to 63 months); the results of those still receiving protriptyline were compared with those who stopped using the drug. Nine patients were still receiving protriptyline at the follow-up visit (10 to 20 mg/day at bedtime), and seven had stopped using the drug because of side effects. These two groups of patients did not differ in their follow-up duration, age, weight, pulmonary functions, and sleep architecture, or in their protriptyline-induced changes in diurnal arterial blood gases and nocturnal desaturation. At the follow-up visit, arterial blood gas determinations had returned to baseline values in all patients no longer receiving protriptyline. In the other group there was no difference between the baseline and follow-up PaO2 values (57.4 +/- 3.4 and 57.0 +/- 1.2 mm Hg, mean +/- SEM). There was no difference in the results of arterial blood gas determinations and pulmonary function tests obtained at the different visits between the two groups. Sleep architecture differed between these two groups, REM sleep time being shorter and the slow-wave sleep time being longer in the patients still receiving the drug. In both groups the cumulative SaO2 curves were similar to those obtained at baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Circadian Rhythm↗
PubMed1993

Effects of protriptyline on snoring characteristics.

We evaluated the effects of protriptyline on snoring characteristics in 14 nonapneic snorers (age range, 23 to 54 years; body mass index, 27.4 +/- 0.9 kg/m2, mean +/- SEM). The study design was a double-blind placebo-controlled crossover trial. Patients were evaluated during a polysomnographic study after each 2 weeks of treatment. Breathing sounds were recorded with two microphones symmetrically placed on each side of the bed, the signal being preamplified, equalized, and analyzed by using a real time analyzer. A snoring event was defined as a breathing sound with a sound pressure level (SPL) greater than 60 dB SPL. The snoring index (number/sleep hour) and the sound intensity of each event were automatically determined. Mild side effects were observed in ten subjects, but no subject interrupted the study because of them. The REM sleep time decreased with protriptyline with a parallel increase in stages 1 to 2. There was no difference in body position during sleep between the placebo and protriptyline trials. The snoring index decreased from 335 +/- 40 with placebo to 238 +/- 41 with protriptyline (p < 0.05) with important individual differences. Among the different sleep stages, the highest values of the snoring index were observed in slow-wave sleep with placebo. The snoring index decreased in each sleep stage with protriptyline, the highest decrease occurring in slow-wave sleep. The percentage of total sleep time (TST) spent above 60 dB SPL was significantly lower with protriptyline (6.1 +/- 1.2 percent TST) than with placebo (8.6 +/- 1.2 percent TST). Changes in snoring characteristics were not correlated with snoring severity, the drug blood level, the body mass index, or the drug-induced modifications in sleep architecture. We conclude that protriptyline can improve both snoring frequency and loudness in some nonapneic snorers, and that this improvement occurs mostly in the sleep stages where snoring is worst.

Acoustics↗
PubMed1990

Effects of protriptyline on diurnal and nocturnal oxygenation in patients with chronic obstructive pulmonary disease.

OBJECTIVE: To determine the effects of a nonsedating tricyclic antidepressant (protriptyline) on pulmonary function (lung volume, expiratory flow), arterial blood gases, sleep architecture, and sleep-induced breathing abnormalities in patients with chronic obstructive pulmonary disease. DESIGN: A before-and-after trial in which patients, blinded to treatment, were given a placebo for 2 weeks, followed by 2 and 10 weeks of protriptyline treatment. SETTING: Referral-based pulmonology clinic in a public institution. PATIENTS: Sixteen outpatients were enrolled in the trial. Complete results for 11 patients and partial results for 3 patients are presented. INTERVENTIONS: Patients were evaluated at baseline, after receiving placebo for 2 weeks, and after 2 and 10 weeks of protriptyline therapy (20 mg/d, taken at bedtime). MEASUREMENTS AND MAIN RESULTS: At baseline, for the whole group, forced expiratory volume in 1 second (FEV1) was 1.0 +/- 0.08 L (mean +/- SE); the partial pressure of O2 in arterial blood (PaO2) was 59 +/- 1.2 mm Hg; and the partial pressure of CO2 in arterial blood (PaCO2) was 48.9 +/- 1.2 mm Hg. These variables remained stable after placebo. Pulmonary function test results were unchanged with protriptyline therapy. Arterial blood gas levels improved with such therapy: PaO2 levels increased by 5.1 +/- 1.4 mm Hg after 2 weeks and 6.7 +/- 2.4 mm Hg after 10 weeks (P less than 0.01); PaCO2 levels decreased by 4.2 +/- 0.9 mm Hg after 2 weeks and 2.2 +/- 1.1 mm Hg after 10 weeks (P less than 0.01). Total sleep times were similar at these visits. The only change in sleep architecture was a significant decrease in rapid eye movement (REM) sleep. The lowest value for the saturation of hemoglobin with O2 in arterial blood (SaO2) seen during sleep was 72.0% +/- 2.0% at baseline. After 2 and 10 weeks of protriptyline therapy, SaO2 values increased by 7.1% +/- 1.6% and 5.0% +/- 2.1%, respectively (P less than 0.01). With protriptyline therapy, the cumulative SaO2 curve, derived from data obtained during sleep, shifted down and to the right. CONCLUSIONS: Protriptyline improves diurnal and nocturnal hypoxemia in patients with chronic obstructive pulmonary disease. These changes are not related to changes in pulmonary mechanics.

Circadian Rhythm↗
PubMed1992

Further characterization of reversal of signs of induced cotton effects of dicumarol derivatives-alpha 1-acid glycoprotein systems by protriptyline.

The interaction of dicumarol derivatives and protriptyline with respect to the binding to alpha 1-acid glycoprotein (AGP) has been investigated by circular dichroism (CD), equilibrium dialysis and ultrafiltration. Investigation of the induced CD spectra of dicumarol derivatives bound to AGP indicated that the conformations of these compounds were different when bound to AGP. Though all the dicumarol derivatives, protriptyline and AGP formed a ternary complex, interaction modes were different, depending upon the substituent groups at position 3 of the dicumarol molecule. On the basis of the protriptyline effect on the CD spectra of all dicumarol derivatives bound to AGP, the compounds were classified in the following way: (1) Dicumarol, ethylidenebis 4-hydroxycoumarin and propylidenebis 4-hydroxycoumarin caused reversal of the sign of ellipticity. This interaction was explained by cooperative binding. (2) Butylidenebis 4-hydroxycoumarin and pentylidenebis 4-hydroxycoumarin generated new band and disappeared ellipticity of the original Cotton effect. This interaction was also explained by the cooperative binding mode. (3) Ethylbiscoumacetate which generated the CD band similar to that of dicumarol in the absence of protriptyline, reversed the sign of the CD spectrum only at 325 nm. The interaction was anticooperative in nature. (4) Benzylidenebis 4-hydroxycoumarin represented type four which had no change in the CD spectrum by the addition of protriptyline. This interaction was explained by the two-state model accompanying the conformational change of AGP. These results suggested that all compounds, except for benzylidenebis 4-hydroxycoumarin, induced negative Cotton effects at 325 nm by taking the same asymmetrical perturbation by the addition of protriptyline and the interaction was carried out according to model 2. An attempt to study the interaction mechanism of two or more drugs with regard to the binding to protein using these models is thought to help in understanding drug-protein interactions.

Binding Sites↗
PubMed1996

A naturalistic assessment of protriptyline for attention-deficit hyperactivity disorder.

OBJECTIVE: To evaluate the potential benefit of the tricyclic antidepressant, protriptyline, in the treatment of children and adolescents with attention-deficit hyperactivity disorder (ADHD). METHOD: All clinic patients in an outpatient pediatric psychopharmacology unit treated with protriptyline for ADHD were monitored for response to treatment. Thirteen subjects (11 male, 2 female) were treated naturalistically with protriptyline for ADHD and were administered the ADHD Symptom Rating Scale and Clinical Global Impression of Severity (CGI-S) and improvement (CGI-I) at baseline and while taking medication. All patients had failed to respond to at least one previous medication trial, and 46% had psychiatric comorbidity. RESULTS: Patients received an average protriptyline dose of 17 mg (range 5 to 30 mg) for 11.5 +/- 6.8 weeks. Of the 11 patients who continued to take protriptyline for at least 4 weeks, there was a modest reduction in the ADHD symptom checklist (p < .004) and the CGI-S (p = .032). However, using a predefined criteria of response, only 45% of patients were considered positive responders. Adverse effects were prominent, with 46% of patients reporting clinically significant problems and 38% of patients discontinuing treatment because of intolerable side effects. CONCLUSION: These findings do not support the clinical utility of protriptyline in the routine management of complex cases of ADHD in children and adolescents. However, the usefulness in noncomorbid, medication-naive ADHD individuals remains unclear.

Ambulatory Care↗
PubMed1977

Plasma concentrations and cardiotoxic effects of desipramine and protriptyline in the rat.

1 Desipramine and protriptyline were administered to anaesthetized rats by two consecutive intravenous infusions in order to obtain a peak level (first infusion) followed by lower steady state concentrations (second infusion) (Wagner, 1974). Theoretical plasma level time courses were confirmed experimentally.2 Desipramine and protriptyline were measured in atria and ventricles. Increasing infusion rates led to proportional increases in plasma and atrial concentrations. The tissue/medium ratio ranged from 57 to 21 for desipramine and from 43 to 11 for protriptyline according to the time of determination during infusions.3 Heart rate changes, deviation of the electrical axis of the heart and prolongation of atrioventricular conduction were recorded at fixed times during infusion.4 Positive chronotropic effects were noted at plasma concentrations ranging from 0.035 to 0.1 mug/ml for desipramine and from 0.04 to 1.2 mug/ml for protriptyline. At higher plasma concentrations the positive chronotropic effect decreased and bradycardia developed. Both drugs induced right rotation of the electrical axis of the heart. Threshold plasma levels giving 40 degrees rotation were 1.35 mug/ml (desipramine) and 1.75 mug/ml (protriptyline). Atrioventricular conduction was prolonged at threshold plasma concentrations of 2.2 mug/ml for desipramine and 3.6 mug/ml for protriptyline.5 Desipramine is more cardiotoxic than protriptyline. This difference is discussed in relation to the plasma and heart concentration of the two drugs.

Animals↗
PubMed1989

Changes in day and night time oxygenation with protriptyline in patients with chronic obstructive lung disease.

The effect of protriptyline, a tricyclic antidepressant, on sleep architecture, nocturnal arterial oxygen desaturation, pulmonary function, and diurnal arterial blood gases was investigated in an open study of 14 patients with stable chronic obstructive lung disease. Daytime and overnight measurements were made before and 2 and 10 weeks after they started protriptyline (20 mg daily at bedtime). Two patients had to be excluded before the second visit and one before the third visit because of changes in treatment for their chest disease. Protriptyline caused mouth dryness in all patients and dysuria in six men. With protriptyline there were no significant changes in total sleep time, sleep period time, or the percentages of total sleep time occupied by stage I-II and stage III-IV sleep. The mean (SEM) percentage of total sleep time spent in rapid eye movement (REM) sleep decreased from 11.1 (1.7) to 4.6 (0.7) at two weeks and to 4.2 (1.0) at 10 weeks. After protriptyline the time spent during sleep with an arterial oxygen saturation (SaO2) below each 5% increment above 65% was less than the baseline time; the lowest SaO2 (%) reached during sleep increased from 64.5 (1.7) to 72.7 (2.1) at 2 weeks and to 77.4 (2.1) at 10 weeks. Lung volumes and expiratory flows were unchanged during the study. Daytime arterial oxygen tension (PaO2) increased from 57 (1.4) mm Hg before treatment to 62 (1.9) mm Hg at 2 weeks and to 66 (1.9) mm Hg at 10 weeks (7.6 (0.2), 8.3 (0.3), 8.8 (0.3) kPa). Carbon dioxide tension fell from 52 (2.3) mm Hg to 49 (1.4) mm Hg at 2 weeks and to 48 (2.0) mm Hg at 10 weeks (6.9 (0.3), 6.5 (0.2), 6.4 (0.3) kPa), but these changes were not significant. These results suggest that protriptyline may benefit patients with chronic obstructive lung disease by reducing the sleep induced falls in SaO2 and improving diurnal PaO2; a controlled trial is now required.

Aged↗
PubMed1995

Effect of protriptyline, 10 mg daily, on chronic hypoxaemia in chronic obstructive pulmonary disease.

A daily dose of 20 mg of protriptyline can improve daytime arterial blood gas tensions in chronic obstructive pulmonary disease (COPD). Its usefulness is limited by anticholinergic side-effects. This study examined whether a daily dose of 10 mg of protriptyline improved daytime arterial oxygen tension (PaO2) and quality of life in patients with stable mild or moderate hypoxaemia caused by COPD. Twenty six patients were randomized to receive protriptyline or placebo in a double-blind parallel-group trial for 12 weeks, following a run-in period of 4 weeks, in order to assess the stability of hypoxaemia. Patients with a change in PaO2 of > 0.7 kPa during the run-in were excluded. Spirometry, quality of life and dyspnoea score were measured at randomization and after 12 weeks, whilst arterial blood gas tensions were also measured 2 and 6 weeks after randomization. No improvement in arterial blood gas tensions, spirometry values, dyspnoea score, or quality of life was found in either the protriptyline or the placebo group. The majority of patients receiving protriptyline experienced anticholinergic side-effects, which necessitated the withdrawal of the drug in one patient. We conclude that there was no evidence that a daily dose of 10 mg of protriptyline had a significant effect on daytime arterial oxygen tension in stable mild and moderate hypoxaemia caused by COPD. Despite the low dose, anticholinergic side-effects occurred in most patients.

Aged↗
PubMed1985

Effects of short- and long-term protriptyline treatment on phospholipid metabolism in rat brain.

Wistar rats were injected intraperitoneally with 10 mg/kg of protriptyline according to one of the following schedules: a single dose or daily for 4 days (short-term), or daily for 2 or 13 weeks (long-term). Total lipid, total phospholipid, and individual phospholipid contents in the brain were determined. Further, the incorporation of 32P into individual phospholipids in vivo and the fatty acid composition of phosphatidylethanolamine in the brains of rats treated with protriptyline for 13 weeks were studied. Three alternative phases of changes of total and individual phospholipid contents in the brain during 13 weeks of experimentation were distinguished. An increase of phospholipid contents after 4 days, a decrease after 2 weeks, and a further increase after 13 weeks of protriptyline administration were found. However, phosphatidylinositol and phosphatidic acid levels after 13 weeks of protriptyline administration were diminished. The decrease of specific radioactivity of phosphatidylethanolamine, phosphatidylcholine, and phosphatidylserine and the increase of phosphatidylinositol, phosphatidic acid, and sphingomyelin in rats treated with the drug for a longer period of time were noted. No greater differences in fatty acid composition of phosphatidylethanolamine in the brains of the same group of rats were observed as compared to control. These results indicate that during long-term treatment with protriptyline the contents of lipids and phospholipids in rat brain are altered. The modification of the biological function of phospholipids in brain cell membranes is suggested.

Animals↗
PubMed1991

Response of obstructive sleep apnea to fluoxetine and protriptyline.

Protripyline is the pharmacologic agent most commonly used to treat obstructive sleep apnea (OSA); however, its anticholinergic side effects make it intolerable to many patients. Because serotonin may be a central respiratory stimulant and because the serotonin-uptake inhibitor, fluoxetine, is usually well tolerated, we wanted to try fluoxetine in the treatment of OSA. Therefore, we compared the effect of fluoxetine to that of protriptyline in 12 patients with OSA. Both drugs significantly decreased the proportion of REM sleep time and decreased the number of apneas or hypopneas in NREM sleep. The response to fluoxetine was equivalent to that of protriptyline; however, for the group as a whole, there was no significant improvement in the number of arterial oxygen desaturation events, the level of arterial oxygen desaturation, or the number of arousals with either agent. Although there was wide variability in the response to each medication, six of the 12 patients had good responses, including improvement in oxygenation, to either fluoxetine or protriptyline. Three patients could not complete the trial of protriptyline. We conclude that fluoxetine is beneficial to some, but not all, patients with OSA. Fluoxetine was better tolerated than protriptyline.

Adult↗
PubMed1977

Pharmacokinetic aspects of protriptyline plasma levels.

Plasma levels of protriptyline have been determined in 30 patients undergoing antidepressant therapy. After 3 1/2 weeks treatment at dosage levels of 40 mg/day, protriptyline plasma levels ranged from 430 to 1430 nmol/l. During this period only two-thirds of the subjects had definitely achieved asymptotic concentrations. Single dose studies in 5 volunteers suggest that the volume of distribution of protriptyline shows little intersubject variation. The half life of the drug, however, may vary appreciably from subject to subject, ranging from 54 to 198 h. The effects of two sedatives on mean protriptyline plasma levels have been determined. Mean plasma levels for nitrazepam recipients are indistinguishable from those for patients receiving no night sedation. The mean plasma levels for a group of patients receiving sodium amylobarbitone were significantly reduced. The problems of choice and early adjustment of dosages in order to achieve satisfactory plasma levels is discussed. For practical purposes it is suggested that early values may be of predictive significance in allowing early dosage adjustments to be made.

Administration, Oral↗
PubMed1980

The effects of chlorimipramine and protriptyline on tube running activity in mice.

We have developed a new technique, tube running activity, to study the effects of drugs on a specific behaviour in mice. The time it takes for a mouse to run 100 cm in a narrow tube is measured. The effects on tube running activity of chlorimipramine, a relatively specific blocker of the amine pump in the 5-hydroxytryptaminergic neurons, and protriptyline, a relatively specific blocker of the amine pump in the noradrenergic neurons, were studied. During the first two hours after the administration of chlorimipramine 7.5 mg/kg IP there was a decreased run time as compared with controls. The run time could not be further decreased by increasing the dose of chlorimipramine, but the effect was prolonged. Protriptyline in the dose range of 3.75-30 mg/kg IP had no observable effect on the run time, but protriptyline 60 mg/kg IP decreased the run time in the same way as chlorimipramine 60 mg/kg IP did. The decreased run time after protriptyline 60 mg/kg IP is probably due to a blockade of the amine pump in the 5-hydroxytryptamine neurons at this high dose. Our results suggest that tube running activity more specifically measures functional effects of 5-hydroxytryptamine than functional effects of noradrenaline.

Animals↗
PubMed1999

Biotransformation of protriptyline by filamentous fungi and yeasts.

1. The potential of various fungi to metabolize protriptyline (an extensively used antidepressant) was studied to investigate similarities between mammalian and microbial metabolism. 2. Metabolites produced by each organism were isolated by high-pressure liquid chromatography and identified by nuclear magnetic resonance and mass spectrometry. The metabolites identified in one or more fungi were 2-hydroxyprotriptyline, N-desmethylprotriptyline, N-acetylprotriptyline, N-acetoxyprotriptyline, 14-oxo-N-desmethylprotriptyline, 2-hydroxy-acetoxyprotriptyline and 3-(5-hydrodibenzo[bf][7]annulen-5-yl)propanoic acid. 3. Among 27 filamentous fungi and yeast species screened, Fusarium oxysporum f. sp. pini 2380 metabolized 97% of the protriptyline added. Several other fungi screened gave significant metabolism of protriptyline, including Cunninghamella echinulata ATCC 42616 (67%), C. elegans ATCC 9245 (17%), C. elegans ATCC 36112 (22%), C. phaeospora ATCC 22110 (50%), F. moniliforme MRC-826 (33%) and F. solani 3179 (12%). 4. F. oxysporum f. sp. pini produced phase I and phase II metabolites and thus is a suitable microbial model for protriptyline metabolism.

Animals↗
PubMed1986

Treatment of narcolepsy: objective studies on methylphenidate, pemoline, and protriptyline.

Methylphenidate, pemoline, and protriptyline were studied for their treatment efficacy in narcolepsy. A low, intermediate, and high dose level of each drug was studied for 1 week. For methylphenidate the doses were 10, 30, or 60 mg/day; for pemoline, 18.75, 56.25, or 112.5 mg/day; and for protriptyline 10, 30, or 60 mg/day. The order of dose levels was random from subject to subject and the daily dose was divided into thirds and taken in identically appearing capsules morning, noon, and afternoon. Subjects were 6 narcoleptic patients studied on methylphenidate (5 women and 1 man; mean age 54.5 + 11.7 years), 7 narcoleptic patients studied on pemoline (5 women and 2 men; mean age 43.0 + 7.1 years), and 4 narcoleptic patients studied on protriptyline (2 women and 2 men; mean age 42.5 + 16.9 years). Testing consisted of day-long sessions occurring at the end of each dose level and involving a clinical status questionnaire as well as maintenance of wakefulness, Wilkinson addition, and Digit-Symbol Substitution tests. Results were compared with 9 control subjects with no sleep disorder (5 women and 4 men; mean age 39.2 + 8.4 years) who were given placebo that was purported to be a "stimulant drug" and tested in a similar manner. Results demonstrated profound differences in ability to stay awake and perform between narcoleptic patients and controls. Data also suggested that methylphenidate significantly improves ability to stay awake. Pemoline seems to improve ability to perform. Protriptyline does not significantly alter ability to stay awake or to perform.

Adult↗