Hypoxic Pulmonary Vasoconstriction and Gas Exchange During Exercise: DISCUSSION part 2
Role of HPV During Exercise
At rest, nifedipine diverted blood flow to poorly ventilated lung units (Fig 1 and 3). This observation strongly suggests release of HPV and is in keeping with previous reports in COPD. After releasing HPV, the increase in Ppa seen during exercise was blunted and the severity of pulmonary hypertension was lowered (Fig 2), again in accordance with former investigations. To our knowledge, however, the effects of this lowered vascular tone on the adaptation of Va/Q mismatching to exercise in COPD have not been previously investigated. Our results show that the dispersion of the blood flow distribution (LogsD Q) was always higher after than before nifedipine, either at rest or during exercise (Table 2 and Fig 3). Moreover, in contrast to before nifedipine conditions, the Vd/Vt ratio did not fall with exercise after nifedipine (Table 2). As a result, Vd/Vt during exercise was higher after than before nifedipine (Fig 3). The reason for this latter finding is not evident but a possible explanation is as follows. Nifedipine theoretically exerts its maximal vascular effect on those lung units with more alveolar hypoxia. Therefore, it could be expected that during exercise after nifedipine, hypoxic areas would receive more blood flow than those units with normal and high Va/Q ratios, making the latter less well perfused and, as a result, increasing their Va/Q ratio. Taken together, these two observations (higher LogsD Q, no change in Vd/Vt with exercise after nifedipine) indicate that the release of HPV induced by nifedipine certainly interferes with the ability of the pulmonary circulation to efficiently control the distribution of blood flow during exercise. However, it also appears from our results that this has a small effect in modulating the gas exchange response to exercise in COPD. Note that the overall amount of Va/Q mismatching (DISP R-E*) improved with exercise even after the release of HPV induced by nifedipine (Table 2). Graphically, this is shown by the virtual disappearance of the low Va/Q mode in the blood flow distribution in all of the patients in whom it had appeared at reast after nifedipine (Fig 1). Moreover, since exercise lowered the dispersion of the blood flow distribution (LogsD Q) irrespective of nifedipine (ie, with or without modifying the pulmonary vascular tone) (Fig 3), we suggest that most of the Va/Q improvement seen during exercise is due to improvement of the ventilation distribution.
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For example, the increase in the end-inspiratory volume that follows exercise may have facilitated a better ventilation of airways that were partially closed at rest. We cannot exclude that nifedipine has some effect on the bronchomotor tone. However, given that nifedipine has no bronchodilator effect at rest in asthmatic patients, we consider unlikely that it may have had any effect in our patients who have irreversible airflow limitation. Alternatively, nifedipine might have theoretically prevented the development of some bronchoconstriction induced by exercise. However we found that, before nifedipine, exercise improved Va/Q inequality, an observation that is at variance with the hypothesis of exercise-induced bronchoconstriction. Further, during exercise after nifedipine we showed more Va/Q mismatch than before nifedipine. If we speculate that nifedipine really has either a bronchodilator or a protective effect on the bronchial tone, then it would be conceivable to observe a better Va/Q matching after its administration, which was not shown. In summary, it seems highly unlikely that nifedipine had any effect on the bronchomotor tone in our patients. On the other hand, the potential effects of the slight changes in C02 during exercise on bronchomotor or vascular tone, although presumably negligible, cannot be quantified be design.
To summarize, our study shows that exercise can improve Va/Q mismatching in COPD, although the type of response (te, improvement or no change in the Va/Q maldistribution) is probably related to the severity of COPD. Further, it suggests that most of this improvement depends on a more homogeneous distribution of the inspired ventilation and that hypoxic pulmonary vasoconstriction probably plays a minor role in the modulation of such response. Nevertheless, our results also demonstrate that the release of hypoxic pulmonary vasoconstriction by nifedipine interferes with the ability of the pulmonary circulation to distribute blood flow more efficiently and worsens pulmonary gas exchange, not only at rest but also during exercise. Finally, this investigation highlights a limitation in the diffusion of Oz from the alveoli to the end-capillary blood during exercise of COPD. Undoubtedly, this observation requires further investigation. Taken all together, these results help to better understand the mechanisms that govern pulmonary gas exchange during exercise in COPD.
