Acute effects of inhaled isoproterenol on the mechanical characteristics of the lungs in normal man

Abstract

A B S T R A C r We investigated the effects of isoproterenol on the pulmonary mechanics of eight healthy male subjects. We measured the flow-volume, pressurevolume, resistance-volume, and pressure-flow relationships of the lungs of our subjects in addition to the forced expiratory volume (FEV1). The results of this study confirm earlier observations that isoproterenol produces a considerable decrease in airway resistance but only small changes in maximum expiratory flow. Measurements of static pressure-volume curves showed that isoproterenol caused a temporary decrease in the elastic recoil pressure of the lungs. In five men there were mean falls in recoil pressure of 4.1 cm H2O at 85% total lung capacity (TLC), 2.6 cm H2O at 75% TLC, and 1.5 cm HMO at 50% TLC. We postulate that the reason for the relatively small increments in maximum expiratory flow after isoproterenol is primarily that the effects of airway dilatation are in large part negated by the reduction in lung recoil pressure, which results in a fall in the maximum effective driving force for expiratory air flow, and secondly that there is an increase in the compliance of the flow-limiting airways. These studies emphasize that tests of maximum flow and of airway resistance should not be regarded as invariably interchangeable in the assessment of airway reactions or mild disease of the airways.

Relative contributions of large and small airways to flow limitation in normal subjects before and after atropine and isoproterenol.

“…It is of interest to compare in some detail our findings with those of McFadden et al (3). They were the first to point out that changes in Palv' could be used to interpret the distribution of airway resistance changes and, indeed, that such changes, according to EPP concepts, would be related to this distribution and to Pst(l), but unrelated to total airway resistance.…”

“…There was a small yet consistent decrease in air and HeO2 Rus after all three bronchodilator regimens. (3) demonstrated that isoproterenol given in large doses reduced Pst(l). These authors suiggested that this was the basis for the greater increases in airways conductance rather than in maximal flows.…”

“…Widdicombe and associates (1) reported a 42% increase in specific airway conductance after subcutaneous atropine, and Severinghaus and Stupfel (2) demonstrated a 29-47% increase in anatomic dead space after this agent. Aerosolized isoproterenol also increases specific airway conductance and maximal expiratory flow (Vmax)1 (3,4). Thus, there exists bronchial smooth muscle tone that can be lessened with therapeutic agents in normal subjects.…”

Severe bronchospasm during epidural anaesthesia

“…However, histochemical fluorescent techniques have shown an extensive network of catecholamine-containing nerves throughout the tracheobronchial tree [8], but it is not understood how these nerves exert their influence on the bronchial smooth muscle [9]. The sympathetic nervous supply to the adrenal gland is derived from the TI,-L, level.…”

Effects of Bronchodilators on the Behavior of Pulmonary Resistance and Dynamic Compliance as Functions of Respiratory Frequency

“…It seems possible, however, that the interference of other factors associated with the bronchodilator treatment may counteract the effects predicted on the basis of the model originally proposed by Otis et al [18]. Because of the existence of bronchomotor tone in normal airways, which can be influenced by atropine or other bron chodilators [10,16,23,24], selective bronchodilation of high-resistance lung units seems unlikely. Participation of low-resist ance units in the response should tend to minimize the effects of bronchodilators on regional time-constant inequality; however, this mechanism can even be expected to ac centuate the inequality if the regional in crease in resistance results from organic changes in the airways rather than from bronchospasm, so that the response of the low-resistance units to the bronchodilator may be relatively more marked than that of high-resistance units.…”