Late Abstracts

Abstract

Cough can occur in patients taking angiotensin converting enzyme (ACE)inhibitors due to the stimulation of airway rapidly adapting receptors by increased levelsof bradykinin which is degraded by ACE. Hypoxia has been reported to decrease ACE activity. METHODS: 20 healthy volunteers underwent baseline (BL) tests at 700m before being transported to 3800m altitude by road (HA). ACE activity, plasma bradykininconcentration and citric acid cough threshold (CACT) were measured at BL and HALCACT was also measured during the 2 week stay at HA. Forced vital capacity (FVC); transepithelial nasal potential difference (NPD) and electrical impedance tomography (EIT)measurements reflecting respiratory epithelial ion transport and extravascular lung water,respectively, have been published from these same subjects (Mason NP et al, J. Appl.Physiol. Published online Dec 2002). RESULTS: There was no change in ACE activity onascent to altitude (41.87±4.0 vs 41.79± 3.9 mU ml¹, p=0.963) although plasma bradykininlevels fell at HA1 cf BL (0.85±0.4 vs 0.17±0.05 ng ml⁻¹, pO.OOl). CACT fell on ascent toHA (5.2611.03 vs 3.55±0.6 gl⁻¹ p=0.024). There was no correlation between ACE activityor plasma bradykinin and CACT. However Poon analysis of repeated measures during thestay at HA revealed a correlation between CACT and FVC (R²=0.546); EIT (R²=0.292)and NPD (R²=0.212). CONCLUSION: High altitude cough is not caused by changes inplasma bradykinin levels, but Poon correlations between CACT and FVC, EIT and NPDwould be consistent with an aetiological role for subclinical pulmonary oedema due toaltered respiratory epithelial ion transport.