RESUMEN
INTRODUCTION: Exercise induced asthma (EIB) is an acute, reversible, usually selflimiting airways obstruction which sets in after exercise in patients with asthma. One popular mechanism of EIA is the increase in histamine and its metabolites in circulation after exercise, which leads to bronchoconstriction via histamine receptors in bronchi. Chlorpheniramine Maleate is potent, less sedative antihistaminic drug, which acts by inhibiting histamine release from mast cells. It is also said to have anticholinergic properties. The aerosol route of administration of a drug has the advantages of a faster onset of action, fewer side effects, and greater protection against EIB with respect to small airways function. This study was conducted to evaluate the effect of Chlorpheniramine Maleate aerosol inhalation on flow volumes and gas exchange. MATERIALS AND METHODS: 25 established patients of stabilized bronchial asthma (18 to 44 years) with history of EIA attending Allergy OPD, Medical OPD or Chest clinic were included in the present study. Patients were studied for 3 days in a week at the same time of day. Baseline spirometry was done to know test parameters, i.e. FEV1, PEFR and FEF50%. Gas exchange study during rest including minute ventilation (VE), oxygen consumption (VO2), Carbon dioxide produced per minute (VCO2), Respiratory quotient (R) was carried out. Patient was asked to perform exercise on bicycle ergometer. During exercise VE, VO2, VCO2 and R were recorded every 30 seconds. FEV1, PEFR and FEF50% were recorded immediately after and 5 min after completion of exercise. On day 2, same procedure was repeated with saline nebulisation before the exercise. On day 3, aerosolized Chlorpheniramine Maleate was used instead of saline for nebulisation. Values obtained were tabulated and analysed. OBSERVATIONS AND RESULTS: After exercise FEV1, PEFR, FEF50% decreased on all three days, but the fall in these parameters was less on Day III (prior nebulisation with Chlorpheniramine maleate) compared to previous days. There was significant increase in FEV1, PEFR and FEF50% (P<0.01, 0.05 and 0.05 respectively) which was seen 30 mins after inhalation of Chlorpheniramine maleate aerosol compared to placebo. Resting and exercise values of Minute Ventilation (VE), oxygen uptake (VO2) carbon dioxide expired, on all the three days were comparable and statistically not significant by the end of exercise. On day 2 and 3, 'R' as compared to that of day1 was slightly significant during rest and initial minutes of exercise but became insignificant after that till the end of exercise. CONCLUSION: This study shows that Chlorpheniramine causes bronchodilation during resting period by acting on the circulating or tissue histamine in asthmatics which contributes to an increase in resting bronchomotor tone. As there is incomplete inhibition of EIA by Chlorpheniramine, there may be some other associated mediator release for pathogenesis of EIA.
