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J Thorac Cardiovasc Surg 2003;126:1674-1675
© 2003 The American Association for Thoracic Surgery
Letters to the editor |
a Division of Cardiology and Critical Care Medicine, Hospital for Sick Children, University of TorontoToronto, Ontario M5G 1X8, Canada
b National Jewish Medical and Research Center, Denver, CO 80206 USA
Reply to the Editor:
We thank Dr Marczin for his interest in our work1 and the Editor for an opportunity to respond.
The first issue raised concerns the methodology of exhaled nitric oxide (NO) analysis. There are several ways to measure exhaled NO at a constant flow rate in the sedated, intubated, and mechanically ventilated patient. These include syringe aspiration sampling as performed by us,1 tidal breathing profiles, and single-breath controlled-flow techniques.2 The latter is difficult to apply outside the neonatal period. We chose the syringe aspiration sampling method because in our preliminary investigations we found it to be a robust, reproducible technique. Indeed, we confirmed the reproducibility of the method by finding similar changes after cardiopulmonary bypass in a previous study investigating exhaled NO before and after surgical closure of left-to-right shunts in children.3 In the most recent study1 we measured exhaled NO in an identical manner in both groups of patients, which suggests that the observed differences between groups were independent of the method of NO sampling. The results of Tworetzky and colleagues4 are intriguing and fully discussed elsewhere.1
The next concerns raised by Marczin are the anatomic origin of exhaled NO and the relationship to endothelial events. Low exhalation single-breath flow rates (<50 mL/s) are characterized by most exhaled NO arising in airways by diffusion, whereas higher flows contain a larger proportion of NO arising in the distal lung.5,6 The syringe sampling was performed toward the end of a mechanical tidal breath, when flows are high. Thus the exhaled breath will contain a higher proportion of NO arising in the alveolar region than would a slow single-breath exhalation. We suggest that NO produced in the endothelium of the pulmonary capillary bed may enter the alveolar space and is reflected in air sampled distally. Capillary blood volume has been shown to correlate with exhaled NO.7 Notwithstanding the elegant study by Sartori and coworkers,8 which was performed in healthy adults, there is evidence to suggest that endothelial derived NO at least partly contributes to exhaled NO levels in cardiovascular disease.9,10 Indeed, Marczin's published position is equivocal on this subject, sometimes for11 and sometimes against.
The influence of cardiopulmonary bypass on exhaled nitric oxide levels is likely to be complex and dependant on the disease, the surgical procedure performed as well as the timing of the measurements. Thus Marczin's cited examples of adults undergoing lung transplantation12 or coronary artery surgery with bronchoalveolar lavage13 may not be comparable to children with congenital heart disease. Indeed, our study is perhaps unique in that cardiac correction was achieved with the use of bypass in one group and without in another. The changes in exhaled nitric oxide thus can be more certainly attributed to cardiopulmonary bypass than is possible in other studies.
The changes in pulmonary blood flow during cannulation for cardiopulmonary bypass described by Marczin are fascinating, and we are certain his group will have the opportunity to submit them for peer review. However, they are irrelevant to the investigation we undertook and to our conclusions. Stated simply, after closure of an atrial septal defect exhaled nitric oxide either increases or decreases, and it is the method of closure and sequelae (surgery vs transcatheter), rather than the hemodynamic consequence of closure (reduction in pulmonary blood flow) that influences the direction of change.
We agree wholeheartedly with Marczin's call for continued dialog and international consensus, and we look forward to the recommendations of the proposed task force.
References
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