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At least 55 records · Page 3Linked to original sources
PubMed1988

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.

Adult↗
PubMed1993

The carotid body in the motorneuron response to protriptyline.

Protriptyline (PRT) has been shown to preferentially stimulate upper airway inspiratory motorneurons relative to phrenic activity in hyperoxic hypercapnia in the decerebrate cat via a carotid body-independent mechanism. Since previous studies indicated that carotid body stimulation results in preferential activation of upper airway respiratory muscles during both hypercapnia and hypoxemia, we hypothesized that if PRT preferentially stimulated upper airway motorneurons, the mechanism of action might involve the carotid body. We investigated the effect of PRT on carotid body function by comparing the electrical activity of the hypoglossal (HYP) with that of the phrenic (PHR) nerve in carotid sinus nerve intact (CSNI) and CSN-sectioned (CSNX) anesthetized rats, before and after PRT (0.5 mg/kg i.v.), during 100% O2, 15% O2 (N2 balance), and 4% CO2 (O2 balance) administration. The moving time average (MTA) peak inspiratory electroneurogram activities of both the HYP and PHR nerves increased an equivalent amount after PRT injection during hyperoxia, in both CSNI and CSNX rats. During hypoxia, the HYP activity increased significantly more than the PHR activity only in CSNI rats after PRT injection. During hyperoxic hypercapnia, HYP MTAs increased a similar amount in the CSNI and CSNX rats. We conclude that the HYP and PHR respiratory motorneuron pool responses to PRT depend on the blood gas status at the time of drug administration.

Animals↗
PubMed1986

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.

Adult↗
PubMed1989

Protriptyline treatment of sleep hypoxaemia in Duchenne muscular dystrophy.

Protriptyline 20 mg daily reduced the total time spent in rapid eye movement sleep in an open study in four subjects with Duchenne muscular dystrophy. Sleep related hypoxaemia and episodes of desaturation were reduced. Anticholinergic side effects were prominent, however, in these patients, precluding its use for regular treatment.

Adolescent↗
PubMed1976

The reversal of clonidine-induced hypotension by protriptyline and desipramine.

The present paper deals with further studies on the interaction between clonidine and tricyclic antidepressants. The pronounced central hypotensive action of 1 mug clonidine/kg, administered into the left vertebral artery of chloralose-anaesthetized cats was readily reversed by protriptyline (300 mug/kg), infused via the same route shortly after the development of the maximum hypotensive effect of clonidine. In earlier studies it has been demonstrated that pretreatment with tricyclic antidepressants significantly diminishes the central hypotensive action of clonidine. This interaction has been presumed to occur at the level of central alpha-adrenoreceptors, where clonidine would be the agonist and tricyclic antidepressants the antagonist. The present findings suggest that a competitive antagonism at the central level, which can occur in either sense, may be involved.

Animals↗
PubMed1976

Plasma concentrations of protriptyline and clinical effects in depressed women.

We studied the relationship between side effects, clinical outcome and the drug plasma levels in 28 female depressed patients treated with protriptyline. After 3 1/2 weeks treatment, patients with plasma levels within a median range (630 to 900 nmol/l) showed better responses to the drug than patients with plasma levels outside this range. There were no statistically signficant correlations between plasma levels and side effect scores or 'corrected' side effect scores (scores after subtracting pretreatment values) for the group at any time after starting the treatment. But we found positive correlations between plasma levels and 'corrected' side effect scores for the neurotic subgroup after 14 and 21 days of treatment. Other correlations between plasma levels and side effect scores were non-significant.

Adjustment Disorders↗
PubMedDate not supplied

Epoxide metabolites of protriptyline in rat urine.

Two epoxide metabolites of 5-(3-methylaminopropyl)-5H-dibenzo[a,d]cycloheptene (protriptyline) were identified in the urine of rats given 14-C-labeled drug. They were characterized by mass spectrometry, nuclear magnetic resonance spectrometry, and chemical reactivity as 10,11-dihydro-10,11-epoxy-5(3-methylaminopropyl)-5H-dibenzo[a,d]cycloheptene (I) and 10,11-dihydro-10,11-epoxy-5(3-aminopropyl)-5H-dibenzo[a,d]cycloheptene (II). Over twice as much I as II was excreted and together the two metabolites accounted for approximately 40% of the urinary radioactivity.

Animals↗