Ann Thorac Surg 2005;80:1977-1978
© 2005 The Society of Thoracic Surgeons
Correspondence
Reply
Christos Alexiou, PhD, FRCS
a
,
Augustine T.M. Tang, DM, FRCS (CTh)
a
,
David C. Smith, MD, FRCA
a
,
Stuart V. Sheppard, PhD
a
,
Marcus P. Haw, MS, FRCS
a
,
Roz Gibbs, PhD
b
a Department of Cardiac Surgery, Glenfield Hospital, University Hospitals of Leicester, Groby Rd, Leicester, United Kingdom
b Faculty of Biomedical Sciences, University of Portsmouth, Portsmouth, United Kingdom
(Email: alexiou486{at}aol.com; roz.gibbs{at}port.ac.uk).
To the Editor:
Thank you for bringing the interesting letter of Zegdi and Fabiani [1] to our attention. Our prospective randomized study [2] examined the effect of systemic arterial line leukocyte depletion (LD) on the rate of exhaled nitric oxide (NO) after cardiopulmonary bypass (CPB) in two groups of patients undergoing first time elective coronary artery bypass grafting. These patients had good left ventricular function and no pulmonary dysfunction nor other organ dysfunction. The use of LD was the only discriminating feature in the perioperative management of the two groups. The study identified a significant rise of exhaled NO after CPB in both groups, however this rise was significantly smaller in those subjected to LD [2].
The rate of exhaled NO was measured with a real time chemiluminescence analyzer at a constant sampling rate of 250 mL/min in all patients [2]. Moreover, samples were collected during a passive exhalation with the patient paralyzed and unable to make an active respiratory effort that would significantly affect the expiratory flow rate. Importantly, exhaled NO rates were similar in the two groups before CPB, and it is only logical to attribute the intergroup differences in the postoperative CPB levels of exhaled NO to the use of LD during CPB.
It is true that the biggest source of exhaled NO is the upper airways, in particular the nasal cavities. This is why gases were collected through the tip of a Teflon catheter (Logan Research, Northampton, UK) positioned beyond the tip of the endotracheal tube [2]. Analysis of these gases showed a concurrent steep rise in the release of exhaled NO and CO2 (CO2 was also monitored). Of note, considerably higher rates of exhaled NO release were recorded when the tip of the sampling catheter was withdrawn in the nasopharynx or when it was positioned within the nostrils (ie, our unpublished own observations). The rate of NO production by the conducting airways and nasopharynx was not measured. However, on the basis of the previously mentioned reasons, it is highly likely that the obtained values of NO do reflect the amount of NO produced across the alveolar-capillary interface, an anatomical area particularly affected by the inflammatory events that unravel during CPB. It is also worth remembering that the cardinal aim of the study was to evaluate the effect of LD, detecting potential differences between the two groups.
It was not our intention to disappoint Zegdi and his collaborators [3, 4] by not quoting their elegant studies on a rat model. In our article, the studies that were cited mainly examined the effect of CPB on the rate of exhaled NO release in human beings. In these studies exhaled NO was seen to increase, not to change or decrease after CPB [5–10]. The possible causes for the observed discrepancies were discussed, clarifying that exhaled NO levels may not reflect the extent of pulmonary inflammation in patients having severely damaged lungs [2, 11]. Furthermore, in the "Conclusions" section of the artcile it was emphasized that according to our study, "the rate of production of exhaled NO may be a useful marker of pulmonary inflammation in low-risk patients undergoing CABG surgery and having normal preoperative lung function" [2].
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References
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- Zegdi R, Fabiani J-N. Exhaled nitric oxide after cardiopulmonary bypass (letter) Ann Thorac Surg 2005;80:1977.[Free Full Text]
- 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]
- 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]
- 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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- Brett SJ, Quinlan GJ, Mitchell J, Pepper JR, Evans TW. Production of nitric oxide during surgery involving cardiopulmonary bypass Crit Care Med 1998;26:272-278.[Medline]
- Ishibe Y, Liu R, Hirosawa J, et al. Exhaled nitric oxide level decreases after cardiopulmonary bypass in adult patients Crit Care Med 2000;28:3823-3827.[Medline]
- Humpl T, Campbell R, Stephens D, et al. Levels of exhaled nitric oxide before and after surgical and transcatheter device closure of atrial septal defects in children J Thorac Cardiovasc Surg 2002;124:806-810.[Abstract/Free Full Text]
- Tworetzky W, Moore P, Bekker JM, et al. Pulmonary blood flow alters nitric oxide production in patients undergoing device closure of atrial septal defects J Am Coll Cardiol 2000;35:463-467.[Abstract/Free Full Text]
- Brett SJ, Evans TW. Measurement of Endogenous nitric oxide in the lungs of patients with the acute respiratory distress syndrome Am J Respir Crit Care Med 1998;157:993-997.[Abstract/Free Full Text]
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