Effects Of Protriptyline Research Articles

Effects of protriptyline on the depletion of catecholamines induced by 6-hydroxydopamine in the brain of the rat.

Effects of protriptyline on the depletion of catecholamines induced by 6-hydroxydopamine in the brain of the rat.

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)

Effects of Protriptyline on Diurnal and Nocturnal Oxygenation in Patients with Chronic Obstructive Pulmonary Disease

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. 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. Referral-based pulmonology clinic in a public institution. Sixteen outpatients were enrolled in the trial. Complete results for 11 patients and partial results for 3 patients are presented. 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). 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. Protriptyline improves diurnal and nocturnal hypoxemia in patients with chronic obstructive pulmonary disease. These changes are not related to changes in pulmonary mechanics.

Effects of protriptyline on vigilance and information processing in narcolepsy.

Vigilance, memory function, and response latency on the Sternberg short-term memory scanning task were examined in eight narcoleptic patients on and off medication. Off medication, half of the patients demonstrated reduced vigilance and all displayed diminished automatic memory encoding and longer response latencies on the Sternberg memory scanning procedure relative to the treated condition. Protriptyline normalized vigilance in half of the patients, while response latency and automatic information processing significantly improved in all. These findings are discussed with regard to the potential effect of the medication on central nervous system arousal.

Effects of protriptyline on sleep related disturbances of breathing in restrictive chest wall disease.

The effects of protriptyline on sleep stage distribution and gas exchange have been assessed in eight patients with nocturnal hypoventilation secondary to restrictive chest wall disease. At a dose of 10-20 mg taken when they retired the total sleeping time was unaltered but the proportion of rapid eye movement (REM) sleep fell from 22% to 12% (p less than 0.05). The total time spent at an arterial oxygen saturation of less than 80% decreased (p less than 0.01) and the magnitude of the fall correlated with the reduction in REM sleep (r = 0.67, p less than 0.05). There was also a reduction in the maximum carbon dioxide tension reached during the night (p less than 0.01). The arterial oxygen tension measured diurnally increased (p less than 0.05) from a median of 8.0 kPa (60 mm Hg) to 9.0 kPa (67.5 mm Hg), but the carbon dioxide tension and base excess were unchanged. Anticholinergic side effects were experienced by most patients but did not limit treatment.

The effects of protriptyline and clomipramine in vitro on the uptake of 5-hydroxytryptamine and dopamine in human platelet-rich plasma.

The effects of protriptyline and clomipramine, at concentrations of 10(-7)M to 10(-4)M, were studied in vitro on the uptake of 5-hydroxytryptamine and dopamine uptake in human platelet-rich plasma. It was found that the tertiary amine, clomipramine, was a more potent inhibitor of 5-hydroxytryptamine uptake than the secondary amine, protriptyline. The activity of both compounds was competitive but it was thought unlikely that they acted through tryptamine receptor sites as methysergide 2.5 X 10(-8)M had very little effect on 5-hydroxytryptamine uptake. Neither tricyclic antidepressant had any marked effect on dopamine uptake.

On the β-hydroxylation of (±)-α-methyldopamine in vivo

Tritium-labelled (±)- a-methyldopamine was given i.v. to mice. The amine was taken up by the heart and converted to 3H- a-methylnoradrenaline. The hydroxylation product seemed to have the erythro configuration. It is suggested that only (+)- a-methyldopamine is β-hydroxylated. The effects of protriptyline, reserpine, sodium diethyldithiocarbamate (DDC) and bis(4-methyl-l-piperazinylthiocarbonyl)disulphide (EWP 815), which inhibit the amine-transport mechanism of the cell membrane of the adrenergic neuron, the granular amine-storage mechanism and the enzyme dopamine β-hydroxylase, respectively, were investigated. In contrast to earlier in vitro observations blockade of the granular storage-mechanism by reserpine caused no corresponding decrease in dopamine β-hydroxylase activity in vitro. Nialamide caused release of 3H- a-methyldopamine, probably by an indirect action, caused by accumulation of endogenous monoamines. Inhibition of catechol- O-methyl transferase by a-propyldopacetamide (H 22/54) caused a twofold increase in the levels of both a-methylated catecholamines in the heart.