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Ann Thorac Surg 2005;80:1977
© 2005 The Society of Thoracic Surgeons

Correspondence

Exhaled Nitric Oxide After Cardiopulmonary Bypass

Rachid Zegdi, MD, PhD, Jean-Noël Fabiani, MD

Université René Descartes–Paris V, Department of Cardiovascular Surgery, Georges Pompidou European Hospital, 20, rue Leblanc, Paris, 75908 France

(Email: rzegdi{at}hotmail.com).

To the Editor:

We read with interest the article by Alexiou and colleagues [1]. Our team has been invested for many years in the noninvasive monitoring of lung inflammation, especially in the context of cardiopulmonary bypass (CPB). The authors reported that in a human study leukodepletion reduced the increase in alveolar production of exhaled nitric oxide (eNO) after CPB. However, before recognizing the beneficial "lung protective" effect of this treatment, there are some concerns with the study that should be clarified.

Nitric oxide (NO) measurements were performed on exhaled breath during a passive exhalation, after disconnecting the patients from the ventilator. Expiratory flow is critical for eNO measurements, even in ventilated patients as shown by others [2]. Why the difference between groups regarding eNO excretion rate after CPB should reflect a difference in alveolar NO production rather than a difference in expiratory flow (which was not monitored). For evident anatomical reason, alveolar gas NO content is always contaminated during exhalation by the NO produced within the conducting airways (from which the bulk of NO in exhaled breath originates). Therefore, how is it possible to attribute the observed increase in eNO release to an increase in rate of alveolar production, as stated in the article? In other words, this would have implied that the conducting airways NO production had been determined concomitantly and was found not to have increased. The distinction between alveolar and conducting airway origins of exhaled NO can be determined even in ventilated patients [3].

Finally, the authors found that their study suggested "a link between the systemic or the pulmonary inflammation and the levels of exhaled NO during CPB." We regret that the authors did not mention in their discussion the studies we performed in a rat model, which were specifically designed to investigate the relationship between eNO and lung inflammation during extracorporeal (ECC) [4–5]. We found that ECC was responsible for lung inflammation and an increase in pulmonary inducible NO synthase expression. Exhaled NO was found to increase in two thirds of the rats submitted to a 90-minute ECC, and this increase did not correlate with the severity of the lung injury.


   References
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 References
 

  1. Alexiou C, Tang ATM, Sheppard SV, Haw MP, Gibbs R, Smith DC. A prospective randomized study to evaluate the effect of leukodepletion on the rate of alveolar production of exhaled nitric oxide during cardiopulmonary bypass Ann Thorac Surg 2004;78:2139-2145.[Abstract/Free Full Text]
  2. MarczinNKövesi T, Royston D. Exhaled nitric oxide as a marker of lung injury in coronary artery bypass surgery Br J Anaesthesia 2003;90:101-105.[Free Full Text]
  3. Tornberg DC, Bjorne H, Lundberg JO, Weitzberg E. Multiple single-breath measurements of nitric oxide in the intubated patient Am J Respir Crit Care Med 2003;168:1210-1215.[Abstract/Free Full Text]
  4. Zegdi R, Fabre O, Cambillau M, et al. Exhaled nitric oxide does not reflect the severity of acute lung injuryan experimental study in a rat model of extracorporeal circulation. Crit Care Med 2002;30:2096-2102.[Medline]
  5. Zegdi R, Fabre O, Cambillau M, et al. Exhaled nitric oxide and acute lung injury in a rat model of extracorporeal circulation Shock 2003;20:569-574.[Medline]



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C. Alexiou, A. T.M. Tang, D. C. Smith, S. V. Sheppard, M. P. Haw, and R. Gibbs
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Ann. Thorac. Surg., November 1, 2005; 80(5): 1977 - 1978.
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