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Ventolin Inhaler and Bronchodilator in Asthma Treatment
Lung function prior to each drug administration was similar (Table 2). There were no significant differences for TLC, FRC, FEV,, FVC, Vmax50, Vmax25 or Rl. Both drugs resulted in bronchodilatation (Fig 2). The FE Vt and Vmax50 were significantly increased and Rl significantly decreased after both drugs. The Vmax25 was significantly increased only after fenoterol. There was no significant difference in the magnitude of change produced by either drug for any variable.
Continued bronchodilatation and ventolin inhalers did not occur during the second part of the study as the postbronchodilator FEVb measured on air before He-02 breathing, was similar to the FEVi measured on air following He-02 breathing, approximately 90 to 120 minutes after administration of the drug (4.61 L vs 4.58 L, p>0.05).
Density dependence of maximal flows and resistance were similar before each study. There were no significant changes in the density dependence of flow or resistance after either agent (Fig 3 and 4). Although only density dependence of Vmax at 50 percent VC is shown, the results at other lung volumes were similarly nonsignificant, as were the changes in density dependence of Rl at an inspiratory flow of 1 Us.
The results of this study demonstrate that fenoterol and ipratropium bromide produce similar degrees of bronchodilatation in normal subjects. There was no systematic change in the density dependence of Vmax or Rl with either agent. Therefore, these results do not support the hypothesis that inhaled anticholinergic agents have a preferential site of action on central airways while inhaled adrenergic agents produce peripheral airway dilatation. The main component and key element of asthma treatment is ventolin inhalers for asthma. Do not forget to follow the link and you will find everything you need for asthma treatment.
The hypothesis behind localization of bronchodilatation by changes in density dependence of Vmax and/or Rl rests on the assumption that the total pulmonary resistance consists of a contribution from central airways, where turbulent flow regimens exist in series with peripheral airways where flow is more laminar. If the resistance of the more central airways, where flow is turbulent, contributes significantly to total resistance, higher flow rates and lower pulmonary resistance will be achieved when air is exchanged for a helium-oxygen mixture, owing to the lower density of the latter gas. If a drug acts predominantly on central airways, the relative contribution of a turbulent flow regimen in these airways to overall resistance will decrease and density dependence will decrease. On the other hand, if a drug acts primarily on peripheral airways where flow is laminar, the central turbulent air flow regimen would then contribute more to overall resistance and density dependence would increase.
Indeed, these were the findings of Ingram et al in seven normal subjects following inhaled atropine sulphate and isoproterenol. They measured maximal expiratory flow breathing air and helium before and after inhalation of these agents delivered by aerosol during a two-minute period of tidal breathing. They were able to show that the density dependence of maximal expiratory flow at 40 percent vital capacity decreased consistently after inhaled atropine and increased after inhaled isoproterenol despite equivalent degrees of bronchodilatation on air with both agents.
MacNee et al also measured density dependence of Vmax and were unable to confirm the findings in a study of eight normal subjects in whom ipratropium bromide and salbutamol were administered by metered dose inhaler and five minutes of tidal aerosol breathing; the combination being employed to ensure diffuse distribution of drug.
In the present study, we have re-examined the issue of drug-related site of action with a selective beta adrenergic agent, fenoterol, and the anticholinergic agent, ipratropium bromide, both administered solely by the usual metered dose inhaler. Since Lisboa et al have suggested that density dependence of maximal expiratory flow may not accurately reflect the series distribution of pulmonary resistance due to the complex factors determining maximal expiratory flow, we also measured the density dependence of pulmonary resistance.
There are several possible explanations for the difference between our results and those of Ingram et al. The first possibility involves the drugs in each study. Ingram et al used atropine and isoproterenol, while fenoterol and ipratropium bromide were given in this study. These differences are unlikely to be important; fenoterol is a specific beta-agonist like isoproterenol, although more beta selective, and ipratropium bromide has comparable anticholinergic activity to atropine. However, the feet that our results are similar to those of MacNee et al who also used ipratropium and a selective betas agonist salbutamol, makes it difficult to rule out this explanation.
The second possible source of differences relates to the site of deposition of the inhaled agents. Recent reports have stressed the importance of inhalation pattern to the distribution of the inhaled drug. Slow deep inhalations deposit aerosol within smaller more peripheral airways, whereas inhalation patterns with smaller volumes and higher inspiratory flow rates tend to deposit the drug in more central zones. Our subjects, inhaling slowly from RV to TLC, would tend to deliver more drug to the peripheral airways; on the other hand, subjects in the study of Ingram et al breathed tidally from a face mask and the smaller volumes could have resulted in more central deposition of drug. Inspiratory flow rates also contribute to the deposition pattern with fester flow rates depositing the aerosol more centrally than slower rates. These characteristics have been exploited in clinical studies to alter the effect of inhaled bronchoactive agents. Aerosol size also alters particle deposition with larger particles distributed more centrally than smaller particles. Metered dose inhalers generally produce particles of uniform size (0.5 to 2.0 μm) which penetrate more peripherally than the larger particles generated by nebulizers.
Thus, changes in the site of bronchodilatation could be influenced by changes in inhalation technique and particle size which may alter the site of drug deposition. In an attempt to circumvent this, MacNee et al used both the metered dose inhaler and tidal aerosol inhalation to deliver the drug and found results similar to the present study as regards density dependence of maximum expiratory flow.
The third potential source of discrepancy between studies relates to variation in the measurement of density dependence of Vmax. A number of studies have questioned the usefulness of the test owing to the marked variability of measurements. The coefficient of variation for AVmax may be greater than 20 percent. Part of this variability stems from the irregular shape of the flow volume curve itself and the necessity to match two curves (one air and the other He-Oa) at a constant lung volume.
Measurement of the density dependence of Vmax may not reflect the series distribution of total airway resistance, but rather may reflect the flow regimen at the site of flow limitation. Recent experimental and clinical studies have questioned the usefulness of AVmax in localizing the site of airway obstruction. Many patients with advanced airflow obstruction in whom peripheral resistance is presumably greatly increased demonstrate well preserved density dependence of Vmax presumably because flow limiting sites remain in large airways where convective acceleration and turbulent flow are important. Lisboa et al have shown that the density dependence of Vmax and Rl did not correlate in a group of asthmatic subjects, and they suggested that the density dependence of tidal resistance would better reflect the distribution of resistance in the tracheobronchial tree.
We did not observe a systematic change in ARl with either bronchodilator and thus our results with Vmax and Rl are consistent in not supporting a preferential site of action for either class of bronchodilator in these normal subjects. It is possible, of course, that a different result would be apparent in patients with asthma.
Thus, in summary, the hypothesis of preferential sites of action of beta-adrenergic agonists and anticholinergic agents is not supported by the results of the current study, at least in normal subjects. Although there is evidence to suggest that receptor densities vary throughout the bronchial tree, the insensitivity of density dependence as a measure of site of resistance and the vagaries governing inhaled drug distribution may have contributed to the negative results of this study.
Table 2—Baseline Lung Function ( ± SD)
Pre Ipratropium Bromide Pre Fenoterol TLC, L 6.40 6.60 .98 .96 FRC, L 3.17 3.35 .46 .43 FVC, L 5.25 5.34 .87 .89 FEV„ L 4.26 4.30 .77 .75 Vmax50, L/s 5.51 5.45 1.02 1.54 Vmax25, L/s 2.21 2.04 .33 .44 Rl, cmH20/L/s 1.53 1.63 .26 .63
Figure 2. Effects of fenoterol and ipratroprium bromide on pulmonary function expressed as the mean percentage change of FEVly Vmax50, Vmax25 and Rl at 1.5 US
Figure 3. Effects of fenoterol and ipratropium bromide on density dependence of Vmax50. Density dependence is defined as the ratio of maximal flow on He-O, to maximal flow on air. Values are mean and standard deviation.
Figure 4. Effects of fenoterol and ipratropium bromide on density dependence of Rl at a flow rate of 1.5 Us. Density dependence is defined as the ratio of Rl on He-Ot to Rl on air. Values are mean and standard deviation.
