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Effects of Fenoterol on Ventilatory Responses to Hypoxia And

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Effects of Fenoterol on Ventilatory Responses to Hypoxia And Thorax 1995;50:139-142 139 Effects of fenoterol on ventilatory responses to hypoxia and hypercapnia in normal subjects Thorax: first published as 10.1136/thx.50.2.139 on 1 February 1995. Downloaded from Yasuhiro Yoshiike, Shunsuke Suzuki, Yuuji Watanuki, Takao Okubo Abstract Lahiri et al' directly measured the carotid Background - The effects of P2 adrenergic chemoreceptor activity and showed that agonists on chemoreceptors remain con- isoprenaline excited the carotid body. Thus, troversial. This study was designed to ex- isoprenaline acts on the P adrenergic receptors amine whether fenoterol, a P2 adrenergic of the carotid body and increases ventilation. agonist, increases the ventilatory re- The effects of 12 adrenergic agonists on the sponses to hypercapnia (HCVR) and hyp- central chemoreceptors remain controversial. oxia (HVR) in normal subjects. Some studies78 showed that 2 adrenergic agon- Methods - HCVR was tested with a re- ists potentiate ventilatory chemosensitivity, but breathing method and HVR was examined this was not a universal finding9 and this dis- with a progressive isocapnic hypoxic crepancy may result from a species difference. method in 11 normal subjects. Both HCVR Furthermore, little is known about the effects and HVR were assessed by the slope of of P2 adrenergic agonists on the ventilatory occlusion pressure (P0.1) or ventilation response to hypoxia. It may be necessary to (VE) plotted against end tidal carbon di- consider the effects of 12 agonists on ventilatory oxide pressure and arterial oxygen sat- control when treating patients with airways uration, respectively. Respiratory muscle obstruction. The purpose of the present study strength, spirometric values and lung vol- was to investigate the quantitative effects of ume were measured. After a single oral fenoterol, a 12 adrenergic agonist, on ventilatory administration of 5mg fenoterol or pla- responses to hypercapnia and hypoxia in nor- cebo HCVR and HVR were evaluated. mal subjects. Results - Fenoterol treatment did not change the specific airway conductance or forced expiratory volume in one second. Methods Respiratory muscle strength did not SUBJECTS http://thorax.bmj.com/ change. Fenoterol increased the slope of Eleven healthy non-smoking men whose mean the HCVR of both Po., (from 0-251 (0.116) (SD) age was 29-0 (6-2) years (range 24-46 to 0-386 (0.206) kPalkPa, average increase years) participated in the study. All were med- 71%) and VE (from 10-7 (3.4) to 15-1 (4-2) ical personnel and had no history of chronic l/min/kPa, average increase 52%), and respiratory or circulatory diseases. All gave in- shifted the response curves to higher val- formed consent and the study was approved ues. For the HVR fenoterol increased the by the institution's committee on investigation slopes of both Po., and VE (from - 4-06 in humans. (2.00) x 10-3 to -7*99 (4.29) x 10-' kPa/ on September 23, 2021 by guest. Protected copyright. %, an average increase of 83%, and from -0-221 (0.070) to -0-313 (0.112) IIminP/o, a 44 5% increase, respectively), and shifted PULMONARY FUNCTION TESTS the response curves to higher values. Spirometric measurements (forced expiratory Conclusion - Acute administration offen- volume in one second (FEVI) and vital capacity oterol increases the ventilatory responses (VC)) were performed using a dry seal spiro- to both hypercapnia and hypoxia in normal meter (OST-80, Chest Co, Tokyo) and body subjects. plethysmography (Autobox 2800, Gould, (Thorax 1995;50:139-142) USA) was used to measure specific airway The First Department conductance (sGaw) and functional residual of Internal Medicine, Keywords: fenoterol, 3 adrenergic agonist, hypercapnic capacity (FRC). Yokohama City ventilatory response, hypoxic ventilatory response. University School of Medicine, 3-9 Fukuura, Kanazawa-ku, VENTILATORY RESPONSES TO HYPERCAPNIA AND Yokohama 236, Japan Isoprenaline, a potent 13 adrenergic agonist, is HYPOXIA Y Yoshiike S Suzuki known to induce hyperpnoeal although the Chemical control of breathing was assessed by Y Watanuki mechanisms underlying this are disputed. measuring minute ventilation (VE) and oc- T Okubo Heistad et all and Winn et al' showed that clusion pressure (PO.,) responses to hypercapnia Reprint requests to: intravenous isoprenaline increased ventilation or hypoxia. Response to hypercapnia (HCVR) Dr S Suzuki. by stimulation of the peripheral chemo- was measured by a modification of the Read Received 21 January 1994 receptors and ventilation was augmented by technique.'0 The circuit used was similar to that Returned to authors 26 April 1994 moderate hypoxia. Wasserman et al' found that of Whitelaw et al." A two way non-rebreathing Revised version received bilateral sectioning of the carotid sinus nerves valve (Hans-Rudolph no. 1400, Kansas City, 6 July 1994 Accepted for publication substantially decreased the ventilatory response USA) was attached to the mouthpiece; both 2 November 1994 to isoprenaline. Eldridge and Gill-Kumar5 and inspiratory and expiratory sides of the valve 140 Yoshiike, Suzuki, Watanuki, Okubo were connected to the rebreathing bag. Mouth P1., and Sao2 (AVE/ASao2 and AP0.,/ASao2, pressure was measured from the side tap of respectively). the mouthpiece using a differential pressure transducer (MP-45 Validyne, Northridge, Thorax: first published as 10.1136/thx.50.2.139 on 1 February 1995. Downloaded from USA). Airflow was measured with a Fleisch RESPIRATORY MUSCLE STRENGTH pneumotachograph (Fleisch no. 1, Lausanne, As we had previously found that fenoterol in- Switzerland) placed between the mouthpiece creased the strength of the fatigued canine and the two way valve. The volume was ob- diaphragm,'3 respiratory muscle strength was tained from electrical integration of the flow assessed by measuring mouth pressures during signal. The inspiratory side of the two way maximal static inspiratory (PImax) and ex- valve was connected with a solenoid valve which piratory (PEmax) efforts against a closed valve was capable of occluding the side of the valve. with a small air leak to prevent glottic closure.'4 The solenoid valve was closed during expiration Pimax was measured at FRC and residual vol- and opened no later than 200 ms after the ume (RV) and PEmax was measured at FRC beginning of inspiration using an analog elec- and total lung capacity (TLC) with a differ- trical circuit, by which a breathing cycle for ential pressure transducer (Validyne MP -45 measurement of occlusion pressure was manu- + 250 mm Hg). The determinations of Pimax ally selected. Occlusion pressure (PO.,) was ob- and PEmax were repeated until three meas- tained from the pressure measured 100 ms after urements varying by <5% and sustained for >2 the onset of inspiration, as defined by the ap- seconds were recorded; the highest value thus pearance of a negative mouth pressure. The obtained was reported. expiratory side was sampled continuously by a mass spectrometer (WSMR-1400; Westron, Chiba, Japan). The resistance ofthe inspiratory PROTOCOL side was 0 059 kPa/l/s, while that of the ex- The study was performed at the same time of piratory circuit was 0 049 kPa/l/s. Subjects day on two different days at least two days wearing nose clips were seated comfortably in apart and within a seven day interval. Subjects front of the rebreathing circuit and held the were instructed to refrain from caffeine-con- mouthpiece in position. Initially they breathed taining beverages, alcohol, and other drugs air by a bypass of the rebreathing bag to room for 24 hours before the study. HCVR was air until the circuit was equilibrated. They then examined in all subjects while HVR was meas- rebreathed a gas mixture of 7% carbon dioxide ured in seven of the 11 subjects. On each test and 93% oxygen from a six litre bag. During day the baseline measurements of pulse rate rebreathing the inspiratory side of the circuit (PR), blood pressure (BP), ventilation and was occluded randomly every 4-6 breaths. Re- PETCO2 were performed at rest. Either 5 mg was continued until the breathing end tidal fenoterol (Boehringer Ingelheim of Japan, http://thorax.bmj.com/ partial pressure of carbon dioxide (PETCO2) Kawanishi, Japan) or placebo was then reached about 8-7 kPa or the subject com- administered orally in a randomised, double plained of dyspnoea. The test was usually blind, crossover design on the first or second terminated within 3-4 minutes. Minute vent- day. Two hours after fenoterol or placebo ad- ilation (VE) was calculated as the average of ministration, pulmonary function tests, res- the two successive breaths preceding the one piratory muscle strength, heart rate, blood used for occlusion. Simultaneously the PETCO2 pressure, ventilation, and PETCO2 were meas- was measured. Hypercapnic response was as- ured and HCVR and HVR were then cal- sessed by the slopes of linear regressions be- culated. For HVR PETCO2 was controlled at on September 23, 2021 by guest. Protected copyright. tween VE and PETCO2 and between Po., and the baseline level before administration of fen- PETCO2 (AVE/APETCO2 and AP0 1/APETCO2, re- oterol or placebo because fenoterol could de- spectively), calculated by the least squares crease PETCO2. The order of the tests (HCVR method. Fifteen to 20 breath pairs were used and HVR) was randomised and at least 10 for analysis. minutes was allowed between tests. Hypoxic ventilatory response (HVR) was measured by a modification of the progressive isocapnic hypoxia method of Rebuck and DATA ANALYSIS Campbell. 12 Subjects rebreathed using the HCVR and HVR varied by approximately 20% same rebreathing circuit as for the hypercapnic and the sample size required to discern a sig- response, except the rebreathing bag contained nificant difference from the drug was 10. All eight litres of a gas mixture of 3-5% carbon values are expressed as the mean (SD). Stat- dioxide, 23% oxygen, and 73-5% nitrogen and istical analysis was performed using the a bypass carbon dioxide absorber was used.
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