HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Guest Access | Sign In via User Name/Password

This Article Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Cataldo, D. Articles by Olivieri, D. Search for Related Content PubMed PubMed Citation Articles by Cataldo, D. Articles by Olivieri, D.

Pathophysiology of a Fall in Arterial Oxygen Saturation During Sputum Induction

Aspirant FNRS Renaud Louis, MD^, ; CHU Sart Tilman Liege, Belgium

Correspondence to: Didier D. Cataldo, MD, Aspirant FNRS, CHU Sart-Tilman, Liege 4000, Belgium; e-mail: didier.cataldo{at}ulg.ac.be

To the Editor:

We were very interested to read the article by Castagnaro et al (October 1999),¹ who have precisely measured, by pulse oximetry, the fall in arterial oxygen saturation (SaO₂) during sputum induction by the inhalation of hypertonic (3%) saline solution. We were surprised by the fact that the fall in SaO₂ was also significant in healthy subjects. In their discussion, the authors suggest that this may be due to a mismatching between ventilation and lung perfusion. Very interestingly, these authors did not find a significant fall in FEV₁, which indicates that no significant bronchial obstruction occurred and, thereby, that bronchial obstruction cannot be considered as an explanation for a sudden mismatch between ventilation and lung perfusion.

Bhowmik et al² studied the falls in FEV₁ and SaO₂ in patients with rather severe COPD and found only slight changes in SaO₂, despite significant falls in FEV₁. This would suggest that the fall in SaO₂ is greater when no clear bronchial obstruction is observed. The hypothesis is that the effect of sputum induction on SaO₂ necessitates a widespread distribution of hypertonic saline solution through the small airways, which is impossible if the patient’s obstructive disease is too severe. In addition, the inhalation of hypertonic saline solution caused a marked fall in SaO₂ in HIV-positive patients who did not have bronchial obstructions and did not develop bronchospasms during the inhalation period.³ Taken together, these data suggest that the hypertonic saline solution acts by modifying the ventilation-perfusion ratio through, modulating the vascular tone. Hypertonic saline solution has been shown to influence the release of neuropeptides⁴ and to induce modifications in the metabolism of arachidonic acid derivatives,⁵ which could explain the vasoactive modifications of small blood vessels in the lung. Consequently, an investigation of the eventual change in lung perfusion should be performed using lung scans of healthy subjects made during the inhalation of hypertonic saline solution.

References

1. Castagnaro, A, Chetta, A, Foresi, A, et al (1999) Effect of sputum induction on spirometric measurements and arterial oxygen saturation in asthmatic patients, smokers, and healthy subjects. Chest 116,941-945[Abstract/Free Full Text]
2. Bhowmik, A, Seemungal, TA, Sapsford, RJ, et al (1998) Comparison of spontaneous and induced sputum for investigation of airway inflammation in chronic obstructive pulmonary disease. Thorax 53,953-956[Abstract/Free Full Text]
3. Miller, R, Buckland, J, Semple, J (1991) Arterial desaturation in HIV-positive patients undergoing sputum induction. Thorax 46,449-451[Abstract]
4. Umeno, E, McDonald, D, Nadel, J (1990) Hypertonic saline increases vascular permeability in the rat trachea by producing neurogenic inflammation. J Clin Invest 85,1905-1908
5. Eggleston, PA, Kagey-Sobotka, A, Proud, D, et al (1990) Dissociation of the release of histamine and arachidonic acid metabolites from osmotically activated basophils and human lung mast cells. Am Rev Respir Dis 141,960-964[ISI][Medline]

Università Degli Studi di Parma Parma, Italy

Correspondence to: Antonio Castagnaro, MD, Istituto di Clinica Delle Malattie Respiratorie, Università Degli Studi di Parma, Viale G. Rasori 10, Parma 43100, Italy; e-mail: respdis{at}unipr.it

To the Editor:

We appreciate the positive comments by Drs. Cataldo and Luis about our study on oxygen desaturation during sputum induction in asthmatics, smokers, and healthy subjects.¹ Furthermore, following the same study protocol, we recently assessed the oxygen desaturation during sputum induction in COPD patients.² In nine COPD patients with mild to moderate airways obstruction, we found that the baseline arterial oxygen saturation (SaO₂) values (mean ± SD), the fall in SaO₂, and change in SaO₂ after sputum induction were 96 ± 2%, 92 ± 3% (p < 0.05), and 4 ± 2%, respectively. Moreover, COPD patients had a small fall in FEV₁ levels (percentage of predicted value) after sputum induction (82 ± 15% vs 77 ± 18%). Like asthmatics, smokers, and healthy subjects, COPD patients had oxygen saturation fall, with no changes in airway obstruction. We think that this drop could be caused by direct deposition of saline solution into peripheral airways, which induces abnormalities of ventilation-perfusion ratios throughout the lung.

To further explain the pathophysiology of SaO₂ fall during sputum induction, Drs. Cataldo and Luis speculated that the hypertonic saline solution might modify the ventilation-perfusion ratio by modulating, vascular tone with a pro-inflammatory mechanism. However, we found that all subjects recovered the SaO₂ fall within 5 min of the cessation of sputum induction, without requiring supplemental oxygen. The transient and self-reversing oxygen desaturation after sputum induction seems, therefore, to be in contrast with a mechanism involving mediators release.

References

1. Castagnaro, A, Chetta, A, Foresi, A, et al (1999) Effect of sputum induction on spirometry and arterial oxygen saturation in asthmatics, smokers, and healthy subjects. Chest 116,941-945
2. Castagnaro, A, Chetta, A, D’Ippolito, R, et al (1999) Effect of sputum induction on transcutaneous oxygen saturation and spirometry in COPD patients. Eur Respir J 14(suppl),518S

This article has been cited by other articles:

				D. Cataldo, J.-M. Foidart, L. Lau, P. Bartsch, R. Djukanovic, and R. Louis Induced Sputum : Comparison Between Isotonic and Hypertonic Saline Solution Inhalation in Patients With Asthma Chest, December 1, 2001; 120(6): 1815 - 1821. [Abstract] [Full Text] [PDF]

This Article Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Cataldo, D. Articles by Olivieri, D. Search for Related Content PubMed PubMed Citation Articles by Cataldo, D. Articles by Olivieri, D.