• T Kövesi, D Royston, M Yacoub, and N Marczin.
• Department of Anaesthetics, Royal Brompton and Harefield NHS Trust, UK.
• Br J Anaesth. 2003 May 1; 90 (5): 608-16.

BackgroundExhaled 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.MethodsBreath-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 micro g kg(-1) intravenous GTN were given by a central venous catheter and exhaled NO and haemodynamic responses were recorded.ResultsIntravenous administration of 1, 2 and 3 micro g 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.ConclusionsThe 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.

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