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British Journal of Anaesthesia, 2003, Vol. 90, No. 5 608-616
© 2003 The Board of Management and Trustees of the British Journal of Anaesthesia


Clinical Investigations

Basal and nitroglycerin-induced exhaled nitric oxide before and after cardiac surgery with cardiopulmonary bypass

T. Kövesi1, D. Royston1, M. Yacoub2 and N. Marczin1,2,3

1 Department of Anaesthetics, Royal Brompton and Harefield NHS Trust, Harefield, UK. 2 Department of Cardiothoracic Surgery, National Heart and Lung Institute, UK. 3 Department of Anaesthetics, Imperial College of Science, Technology and Medicine, Heart Science Centre, Harefield Hospital, Harefield, UK

Corresponding author: Harefield Hospital, Harefield, Middlesex UB9 6JH, UK. E-mail: n.marczin@ic.ac.uk

Background. Exhaled nitric oxide (NO) may reflect NO production and consumption but the pulmonary origin of NO in exhaled gas is not clear. There are also conflicting data on exhaled NO after cardiopulmonary bypass (CPB). Because intravenous nitrovasodilators increase exhaled NO by conversion to NO in the lung, we measured basal and nitroglycerin (GTN)-induced exhaled NO in patients having low-risk coronary artery bypass graft (CABG) operations using routine CPB. We reasoned that GTN-induced exhaled NO would be a primarily vascular mechanism, which would contrast with the airway epithelial origin of basal exhaled NO, and that they might be differentially influenced by CPB.

Methods. Breath-to-breath concentrations of gas phase NO were measured in 12 CABG patients before and 1, 3 and 6 h after CPB. After the baseline measurements, three increasing doses of 1, 2 and 3 µg kg–1 intravenous GTN were given by a central venous catheter and exhaled NO and haemodynamic responses were recorded.

Results. Intravenous administration of 1, 2 and 3 µg kg–1 doses of GTN produced a dose-dependent increase in exhaled NO and a reduction in systemic blood pressure. Baseline exhaled NO remained unchanged. Exhaled NO but not blood pressure responses were reduced 1 and 3 h after CPB.

Conclusions. The capacity of the lungs to increase exhaled NO in response to intravenous GTN is reduced after CPB, suggesting microvascular injury and/or atelectasis after routine open-heart surgery.

Br J Anaesth 2003; 90: 608–16


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