The use of anticholinergic bronchod...

The use of anticholinergic bronchodilators in COPD is based onward the reversal of cholinergic bronchomotor tone. There is little information about the magnitude of cholinergic tone in patients with COPD as compared with normal bring under rules As an index of the amount of cholinergic tone we measured the maximum increase in [FEVsub1] following administration of an optimal dose of the anticholinergic agent atropine methonitrate. The contemplation included nine normal nonsmoking controls ten normal smokers and 22 make submissives with mild to moderately strict COPD. We found that normal nonsmokers had smallest increases in [FEVsub1] following atropine methonitrate administration. rejoinders of subjects with airway disease were progressively greater. Greatest replys occurred in the group of enthralls with prebronchodilator [FEV.sub.1] values les than 55 percent of predicted. The principally plausible explanation for this is that cholinergic tone in COPD is increased in proportion to the severity of airway disease. Other explanations are possible.

In patients with COPD there are several mechanisms of airflow limitation. Many of these are related to destructive and fibrotic changes in the lung which narrow or obliterate the airways. These structural changes are not reversible by the agency of pharmacologic means. However, principally patients with COPD are capable of one bronchodilation,[1,2] and most if not all of the bronchodilatation of which they are capable can be achieved by dint of means of an anticholinergic bronchodilator.[3,4] Patients with COPD thus differ from patients with asthma, who nearly always reply better to an adrenergic bronchodilator.[5] We have remind ofed that one explanation why patients with COPD accord equally well to anticholinergic and adrenergic agents is that, unlike asthmatic exposes the major reversible component of their airways narrowing is that suitable to cholinergic bronchomotor tone.[3] The question arises: in what way much bronchomotor tone is ready in subjects with COPD?

Although it is known from the work of Widdicombe,[6] Nadel,[7] and others that cholinergic components of the parasympathetic system set to work an important degree of have charge of over airway caliber, the amount of cholinergic tone cannot be directly measured in man. However, because atropine-like agents are specific antagonists of the muscarinic drifts of acetylcholine, we reason that it might be possible to make indirect, semiquantitative estimates of cholinergic tone from measuring the increase in airflow when cholinergic tone is abolished with atropine-like agents. Using this course we have compared the amount of bronchodilation resulting from administration of an anticholinergic agent in patients with COPD with that in normal make liables The results are consistent with the hypothesis that cholinergic tone is increased in proportion to the severity of airway disease.

bring under rules AND METHODS

All make subordinates were recruited from Hines VA Hospital. Those with COPD were outpatients who had chronic bronchitis and/or emphysema as defined on recently revised criteria of the American Thoracic Society.[8] All had airflow limitation ([FEVsub1] les than 70 percent of the predicted value) and a history of cigarette smoking equivalent to at least single in kind pack per day for ten years. Patients with any features of asthma, allergies, peripheral eosinophilia or elevated serum IgE on a levels were excluded. None was receiving cromolyn sodium or oral corticosteroids. A replication to bronchodilators was not a condition of note There were 22 patients in this group

Normal controls were recruited from the staff and proffers of the hospital. We included single subjects between 50 and 75 years of age in order to match the age of make submissives with COPD and excluded make liables with any features of asthma or allergies. In this collection there were nine subjects who had in no degree smoked and ten subjects who were instant cigarette smokers and had smok common or more packs per day for ten years.

Each of the 41 make liables was studied on three occasions separated by the agency of at least three days. Those receiving bronchodilators withheld their medications for at least 12 h before the start of each close attention day, 24 h in the case of methylxanthines, and present smokers were asked not to vapor on each day of the studious mood All studies commenced between 7 and 9 AM; after a brief interval period spirometry was performed in duplicate (baseline). The enthrall then inhaled a nebulized solution of atropine methonitrate, 15 mg dissolved in 3 ml isotonic saline solution delivered through a DeVilbiss 645 nebulizer powered at a flow of air at approximately 10 L/min from one side of to the other approximately 5 min. Spirometry was repeated in duplicate at intervals of 05 h for 3 h Atropine methonitrate is a poorly absorbed quaternary kindred of atropine whose effects are confined to the respiratory mucosa when the remedy is inhaled.

A subgroup of the exposes with COPD (baseline [FEV.sub.1] les than 55 percent predicted) was studied forward seven or eight occasions each. The protocol was identical to that described above take exception that body plethysmography was performed immediately preceding spirometry, from which SGaw was determined.