ff ects of fenoterol on ventilatory response to hypercapnia and hypoxia in patients with chronic obstructive pulmonary disease

adrenergic agonists potentiate chemosensitivity whilst another study did not. The ventilatory Background – It has previously been shown that fenoterol, a b2 adrenergic agonresponse to hypercapnia or hypoxia in patients with chronic obstructive pulmonary disease ist, increases the ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) (COPD) continues to be debated. Patients with carbon dioxide retention were found to have a in normal subjects. The effects of b2 adrenergic agonists on chemoreceptors in decreased response to carbon dioxide while non-hypercapnic patients had a normal patients with chronic obstructive pulmonary disease (COPD) remain conresponse. 9 In another study there was no difference in the response to carbon dioxide troversial. This study was designed to examine whether fenoterol increases the between hypercapnic and non-hypercapnic patients. In some studies hypoxaemic patients HVR and HCVR in patients with COPD. Methods – The HCVR was tested in 20 with COPD have been reported to have a decreased response to hypoxia, 12 while in one patients using a rebreathing method and the HVR was examined using a progressive study they had an increased response. The effects of b agonists on ventilation and its chemisocapnic hypoxic method. The HCVR and HVR were assessed by calculating the ical control may therefore be important when b agonists are used to treat obstructive airway slopes of plots of occlusion pressure (P0.1) and ventilation (V̇) against end tidal cardiseases. We have recently shown that fenoterol increases the ventilatory responses to both bon dioxide pressure (P2) and arterial oxygen saturation (Sa2), respectively. hypercapnia and hypoxia in normal subjects. The purpose of this study was to investigate Spirometric values, lung volumes, and respiratory muscle strength were also the effects of fenoterol on the ventilatory responses to hypercapnia and hypoxia in patients measured. The HCVR and HVR were examined after the oral administration of with COPD. fenoterol (15 mg/day) or placebo for seven days. Results – Fenoterol treatment increased Methods the forced expiratory volume in one second Twenty patients (19 men) with COPD of mean (FEV1) and inspiratory muscle strength. (SD) age 67.2 (7.8) years (range 50–80) parIn the HCVR the slope of P0.1 versus P2 ticipated in the study. The patients were diagwas increased by fenoterol from 0.35 (0.23) nosed as having COPD according to the to 0.43 (0.24) (p<0.01). Moreover, the P0.1 definition of the American Thoracic Society. at P2 of 8 kPa was higher on fenoterol All patients were clinically stable and had given than on placebo (p<0.05) and the V̇ was informed consent to participate. The study was also greater (p<0.01). In the HVR fenoterol approved by the Committee on Investigation treatment increased the P0.1 at 80% Sa2 in Humans of our hospital. from 0.90 (0.72) to 0.97 (0.55) kPa (p<0.05) Spirometric tests were performed using a dry while the slopes of the response of P0.1 and seal spirometer (OST-80, Chest Co, Tokyo) V̇ were not changed. and lung volumes were measured using a body Conclusions – Fenoterol increases the plethysmograph (Autobox 2800, Gould, USA). The First Department ventilatory response to hypercapnia in The vital capacity (VC), forced expiratory volof Internal Medicine, patients with COPD, presumably by ume in one second (FEV1), airway resistance Yokohama City stimulation of the central chemoreceptor. University School of (Raw), specific airway conductance (sGaw), The hypoxic ventilatory response is only Medicine, 3–9 Fukura, and functional residual capacity (FRC) were Kanazawa-ku, slightly affected by fenoterol. obtained. Arterial blood was sampled by puncYokohama, Kanagawa (Thorax 1997;52:125–129) 236, Japan ture of the radial artery with the subjects sitting, S Suzuki two hours after drug administration, and gas