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Effect of Protriptyline on Ventilatory Responses to Hypercapnia and Asphyxia in Normal Subjects

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Effect of Protriptyline on Ventilatory Responses to Hypercapnia and Asphyxia in Normal Subjects Eur Respir J 1989, 2, 758-763 Effect of protriptyline on ventilatory responses to hypercapnia and asphyxia in normal subjects A.K. Simonds*, N. Carrell*, M.A. Branthwaite*, N.A. Saunders** Effect of protripty/ine on venJilatory responses to hypercapnia and asphyxia in •Dcpt of Thoracic Medicine, Brompton Hospital, normal subjects. A. K . Simonds, N. Carroll, M. A. BranJhwaite, N. A. Saunders. London, SW3 6HP. ABSTRACT: A double-blind crossover study was undertaken to assess the effect of protrlptyline on ventilatory responses in normal subjects. Seven '"'"The Royal Newcastle Hospital, Newcastle, NSW, Australia, 2300. subjects received in random order placebo, 10 mg and 20 mg protrlptyUne dally for 2 weeks. Measurements of hypercapnic ventilatory response Correspondence: Dr A.K. Simonds, Dept of Thoracic (HCVR) and asphyxial hypoxic ventUatory response (HVR) were made Medicine, Royal Free Hospital, Pond Street, London, before treatment, 6-8 h after the first dose, and after 2 weeks treatment. NW3 2QG. Mean HCVR and HVR following 10 mg and 20 mg protrlptyline did not differ significantly from measurements on placebo, neither for the single Keywords: Asphyxia; hypercapnia; protriptyline; res­ dose study or after 2 weeks. piratory drive. Eur Respir J., 1989, 2, 758-763. Accepted for publication: May 23, 1989. The stimulant tricyclic agent protriptyline decreases hospital Ethics Committee and informed consent was episodic nocturnal desaturation in patients with obstruc­ obtained from participants. tive sleep apnoea [1, 2] and more recently, has been The double-blind, placebo-controlled, crossover trial shown to improve nocturnal gas exchange and diurnal consisted of 3 phases each lasting 2 weeks, with a 2 arterial oxygen saturation in patients with sleep related week washout period between each phase. In random disturbances of breathing secondary to restrictive chest order subjects received placebo, 10 mg protriptyline or wall disease [3) and chronic airflow limitation [4). The 20 mg protriptyline daily for the duration of the phase. mechanism of action of protriptyline in sleep disordered Measurements of HCVR and HVR were made the day breathing has been attributed to a reduction in rapid eye before starting each phase, on the first day of each phase movement (REM) sleep associated episodes of apnoea 6-8 h after ingestion of the tablet (acute study), and after and hypopnoea, with an additional action on upper airway 2 weeks treatment (long term study). After the first day muscle tone [5]. However, an independent respiratory of each phase subjects were requested to take the trial stimulant effect has not been excluded. tablet on retiring. The timing of the studies of both acute This trial was carried out to assess the effect of and long term effects was selected because peak levels protriptyline on hypercapnic and hypoxic ventilatory drive following a single oral dose of protriptyline arc reached in normal subjects. The response to a hypercapnic hy­ after 6-12 hand stable plasma levels are demonstrable in poxic (asphyxial) stimulus rather than to a conventional the majority of subjects after 2 weeks [7, 8). Half-life eucapnic hypoxic challenge was chosen for two reasons. varies between subjects with a mean value estimated at Firstly, hypercapnia potentiates the effect of hypoxia on 78.4 h [9). peripheral chemoreceptors [6] and secondly, as the drug The order of HCVR and HVR was randomised and is being used increasingly in patients with nocturnal measurements were made at the same time of day. The hypoventilalion, hypercapnic hypoxia would seem a more 4 week period between assessments meant the measure­ relevant stimulus. ments were probably made at the same stage of the menstrual cycle in each female subject. Venous samples for de_termination of protriptyline lev­ Subjects and methods els were collected at each measurement session with the exception of the first. Samples were analysed by gas The effect of protriptyline on hypercapnic ventilatory liquid chromatography (10). response (HCVR) and asphyxial hypoxic ventilatory response (HVR) was assessed in seven normal subjects (3 male; 4 female) aged 27-53 yrs (mean age 36.1 yrs). Assessment of ventilatory response Subjects were hospital staff members with no previous experience of the measurement techniques. All were Measurements were made after subjects breathed at nonsmokers with no history of cardiovascular disorders the mouthpiece for 5-10 min until end-tidal carbon and normal spirometry. The study was approved by the dioxide tension (Pco2) was stable. Ventilatory response VENTILATORY RESPONSE TO PROTRIPTYLINE 759 to hyperoxic hypercapnia was determined using a ments of HVR was used for analysis. Ventilatory rebreathing technique [11). Subjects rebreathed for 4 min response to asphyxia was calculated by plotting breath from a 6 I reservoir bag containing 7% carbon dioxide in by breath minute ventilation against arterial oxygen satu­ 93% oxygen. Expiratory flow was intergrated to give a ration at the start of each breath. No attempt was made volume trace using a Fleisch pneumotachograph (size 3) to correct the arterial oxygen saturation reading for the and end-tidal Pco2 was sampled using a Hewleu Packard instrument response time. The position of the HVR line capnometer (model 47201A). The pneumotachograph was determined. by calculating ventilation at a saturation and capnograph were calibrated before each experimen­ level of 95% (V9 ~. tal session with room air and 7% carbon dioxide in 93% Regression lines were only accepted if the correlation oxygen. Calibrations were checked at the end of each coefficient exceeded 0.8. HCVR and HVR before and session. Two sets of measurements of HCVR were made after placebo, 10 mg and 20 mg were compared by 2- at each assessment and the mean of these values was way analysis of variance. Differences between male and used for analysis. To calculate HCVR, measurements female subjects were analysed using the Mann-Whitney 1 during the first 45 s of rebreathing were discarded and test. The correlation between dose (mg·kg· ) and plasma 1 ventilation over subsequent 30 s periods was plolled levels, and dose (mg·kg- ) and side effects was calculated using the Spearman rank correlation test. against the end-tidal Pco2 value at the mid-point of each period. The ventilatory response to hypercapnia, expressed by the slope of this relationship, was calculated by linear regression analysis. The position of the response line was Results established by estimating ventilation ~t an end-tidal Pco2 • HCVR, HVR, V and Y on entry to the trial were of 55 mmHg (7.3 kPa) and termed V55 55 95 The ventilatory response to hypercapnic hypoxia was greater in male subjects than females, although these measured using the method of fuNSLEY and READ [12]. A differences were not significant (p>0.05). controlled decrease in arterial oxygen saturation to ap­ Values before and after placebo, 10 mg and 20 mg proximately 70%, in the presence of a stable elevation of protriptyline are shown in figures 1-4. No placebo effect , Pco2 was obtained by breathing from two reservoir bags was evident and 10 mg and 20 mg protriptyline did not in sequence. From breathing room air, the subject was alter the slope or position of the response curve in both switched into a one-way circuit and rebreathed for 4-5 the acute and long term studies. No trend between breaths from a bag containing 7% carbon dioxide in air. response to 10 mg and 20 mg was observed. Without the subject's awareness he was then switched to Inter-subject variation in pre-treatment data is clearly a second bag containing 7.5% carbon dioxide in nitro­ shown, but no overall difference was seen comparing gen. The expiratory tap was open to air at this stage so initial values for each phase. The coefficient of variation that rebreathing did not occur. When arterial oxygen for control tests was 0.24 for HCVR and 0.37 for HVR. saturation began to fall the subject was switched back to The lower limit of accurate measurement of protrip­ the bag containing carbon dioxide in air and rebreathed tyline using the gas liquid chromatographic method is 1 1 this mixture until the ramp of desaturation was complete. 5 J.Lg·/· • Levels below 5 J.l.&·l· are therefore denoted as Arterial oxygen saturation (Saoz) was monitored continu­ undetectable and assumed to be zero. Plasma protrip­ ously using a Hewlett Packard oximeter model 47201A tyline levels are shown in table 1. 1 whose response to a step change in input from 100-80% No correlation was found between dose (mg·kg' ) is 90% complete in 1.3 s. The mean of three measure- and plasma levels. All subjects noted a dry mouth HYPERCAPNIC VENTILATORY RESPONSE (HCVR) 20 mg Placebo 10 mg fmln''·mmHg·• • 4 ..c: ~ ~ 3 ~ 0 !i 'E 2 ..> c" D. ! Before Altllf Before Alter Beforo After Fig. 1. - Hypercapnic ventilatory response (HCVR) before and after 2 weeks trealment with placebo, 10 mg and 20 mg protriptyline·day·1• Mean values and 95% confidence intervals (Cl) of change in HCVR are shown. 760 A.K. SIMONDS ET AL. HYPOXIC (ASPHYXIAL) VENTILATORY RESPONSE (HVR) fmtn·'·%Sao1·' 4 =c 0 & 10 mg ;r .. PlacebO 2 .. ! 0 0 3 ::r ;r l:' 2 .. '2 .. :::0 :> i C l r+I! "'• "';;• < E.. 2 ;; :IJ .. :I: .. Cl .. < ;u~ :Jl 3 ~ Cl 0 5' .. .!. ~ 3 0. 3 0 .. 0 :> - ~ ~ ~ - ~ - tar • I H~'* z:::: ...!: _, _, ~0t ~i t,.. ...!: :z:: ...!: Before After Before After Before Alter Fig. 2. - Hypoxic (asphyxial) venti.latory response (HVR) before and after 2 weeks treatment with placebo, 10 mg and 20 mg protriptyline·day'. Mean values and 95% confidence intervals (Cl} of change in HVR are shown. Sao1 : arterial oxygen saturation. HYPERCAPNIC VENTILATORY RESPONSE PlacebO 10 mg 20 mg 40 0 ;r '10 ~ "'• 0 ;; < · 20 :: <;: •10 3 3 Before After Before Alter Before After Fig.
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