Is mis-swallowing or smoking a cause of respiratory symptoms in patients with gastroesophageal reflux disease?

Respiratory symptoms were studied in 119 patients operated on for fundoplication and crural repair because of gastroesophageal reflux disease (GERD). The effect of antireflux surgery and of smoking habits on their respiratory symptoms was evaluated. A questionnaire was completed before and after surgery in connection with esophageal investigations. Chronic bronchitis was present in 20% of the patients, 38% of whom were smokers. In the rest of the patients, 18% were smokers. Cough was reported by 34% and expectoration by 21%. After surgery the number of patients with cough and chronic bronchitis was reduced significantly in nonsmokers and to some extent in smokers. It is believed that fundoplication with distal anchoring of the longitudinal esophageal muscle will improve pharyngoesophageal function and thereby decrease aspiration and respiratory symptoms due to mis-swallowing.

Remission of angina pectoris and dyspnea by fundoplication in gastro-oesophageal reflux disease.

This study investigates 113 consecutive patients with gastro-oesophageal reflux disease before and after fundoplication and crural repair with respect to symptomatic improvement of chest pain, angina pectoris, exercise-linked chest pain, meal-linked chest pain, dyspnea, and air hunger, and any correlation between these items and smoking habits. The patients were followed by identical questionnaires completed at the time of oesophageal manometric examination prior to operation and from 6 months up to more than 5 years after operation. There was a highly significant reduction in all kinds of chest pain including angina pectoris, and of dyspnea at follow-up independent of smoking habits. However, air hunger was not significantly reduced. The present results suggest that gastro-oesophageal reflux disease should be taken into consideration in the symptomatic diagnosis of angina pectoris.

Lung permeability in smokers after ambroxol treatment.

There is evidence suggesting the involvement of the surfactant system in the development of lung diseases in cigarette smokers. The aim of the present study was to evaluate the effect of Ambroxol on lung epithelial permeability (LEP) in healthy smokers. Ambroxol is known to stimulate surfactant production. Twenty male patients aged between 20 and 60 years participated in the study. They all smoked at least 15 cigarettes daily for 10 years. We carried out a random double-blind study versus placebo: the drug (Ambroxol 75 mg) or the placebo were given once a day after breakfast for 30 days. Lung permeability was evaluated through scanning pulmonary scintigraphy by inhalation of the polydispersed liquid aerosol diethylenetriaminepentaacetic acid (DTPA), labelled with 99Tc, and delivered by a 'Venticis' system. LEP was expressed as the half-time clearance from the lung of 99Tc-DTPA (T50). The significance of the differences between the two treatments was determined by the Student's test for unpaired data. LEP was not different from the baseline value (T50 = 18.49 min) after placebo administration (T50 = 19.57 min). The patients receiving Ambroxol showed an increased LEP mean value (T50 = 18.36 min) in comparison with the baseline mean value (T50 = 16.41 min). Our results demonstrate that the treatment with Ambroxol was able to decrease LEP in 6 subjects, though not significantly.

Effect of nifedipine on allergen-induced bronchoconstriction.

The effect of nifedipine on allergen-induced asthma in nine asthmatic subjects was studied. All subjects had a history of asthma and positive Prick test; lyophilized allergen extracts of Dermatophagoides Pteronyssinus were used. All solutions were inhaled through DeVilbiss nebulizer. On the first day baseline FEV1 value was measured, allergen extracts were inhaled at increasing doses. The procedure was repeated until a 20% fall from the baseline FEV1 was obtained. Nifedipine or placebo capsules were administered sublingually in a randomized double blind manner. Antigen challenge was given 30 minutes later by using provocating dose of allergen. The change in FEV1 value was calculated from the post nifedipine administration. A significant negative correlation (p less than 0.01) was found between the percentage of protection and the baseline PD20. Nifedipine produced a significant mean change of the bronchial reactivity threshold (p less than 0.01).

Increase in tracheal size with age. Implications for maximal expiratory flow.

Because mechanical properties of central airways play an important role in determining maximal expiratory flow, we examined how tracheal size and maximal expiratory flow changed with age in 50 asymptomatic men, 19 to 61 yr of age, who were lifelong nonsmokers. Cross-sectional area (X-SA) of the intrathoracic trachea was estimated from posteroanterior and lateral chest radiographs taken at full inflation. Maximal expiratory flow-volume curves and spirometry were measured by standard techniques. Tracheal X-SA averaged 2.81 cm2 (SD, 0.38) at mean age 21.1 yr and 3.22 cm2 (SD,0.41) at mean age 52.5 yr, and correlated with peak expiratory flow (PEF) (r = 0.522, p less than 0.001) and FEV1 (r = 0.437, p = less than 0.01) (both expressed as percent predicted values based on age and height). These relationships were weaker than previously described in young men. The results suggest that with increasing age, large airways lose elastic recoil, as previously described for the air spaces. Aging changes in the airways may offset the unfavorable effects of loss of lung recoil and account for the relatively good preservation of PEF and the lack of rise in airways resistance with increasing age.

Abnormal ventilation scans in middle-aged smokers. Comparison with tests of overall lung function.

We have assessed the uniformity of regional ventilation during tidal breathing using continuous inhalation of krypton-81m in 43 male, lifelong nonsmokers and 46 male, current cigarette smokers (mean daily consumption 24.1 cigarettes/day) between 44 and 61 yr of age and with mild or no respiratory symptoms. All subjects had normal chest radiographs. The results of the ventilation scans were compared with tests of overall lung function (spirometry, maximal expiratory flow-volume curves, and single-breath N2 test). Diffuse abnormalities of the ventilation scan were found in 19 (41%) of the 46 smokers but in none of the nonsmokers. Focal abnormalities were found in 7 smokers and 3 nonsmokers. Smokers showed the expected abnormalities in overall lung function (reduced FEV1 and VC, increased single-breath N2 slope, and closing volume), but in individual smokers there was only a weak relation between the severity of abnormality of overall lung function and an abnormal ventilation scan. Abnormal scans could be found when overall lung function was normal and were not invariably found when significant abnormalities in FEV1/VC or N2 slope were present. There was no relation between the presence of chronic expectoration and an abnormal scan. The prognostic significance of an abnormal ventilation scan in such smokers remains to be established.

Effect of a calcium antagonist, nifedipine, in exercise-induced asthma.

The nifedipine effect was studied in 8 extrinsic asthmatic subjects with exercise-induced asthma. Before the exercise the patients received, in a randomized double-blind manner, either 20 mg nifedipine, sublingually or sodium cromoglycate by inhalation on 2 separate days. Nifedipine and sodium cromoglycate in all patients inhibited the exercise fall in FEV1. No differences were found between the two drugs. Nifedipine is a potent antagonist of calcium ion influx in smooth muscle and secretory cells, and these studies suggest that it may inhibit release of mast cell mediators and reduce bronchial smooth muscle contractility in asthma.