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Cardiovascular Research 2007 75(2):434-441; doi:10.1016/j.cardiores.2007.04.019
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Copyright © 2007, European Society of Cardiology

NO metabolite flux across the human coronary circulation

Stephen C. Rogersa,1, Afshin Khalatbaria,1, Borunendra N. Dattab, Sue Elleryc, Vince Paulc, Michael P. Frenneauxd and Philip E. Jamesa,*

aDepartment of Cardiology, Wales Heart Research Institute, School of Medicine, Cardiff University, Cardiff, CF14 4XN, United Kingdom
bDepartment of Medical Biochemistry, School of Medicine, Cardiff University, Cardiff, CF14 4XN, United Kingdom
cDepartment of Cardiology, Ashford and St. Peters NHS Trust, Surrey, KT16 0PZ, United Kingdom
dDepartment of Cardiovascular Medicine, The Medical School, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom

* Corresponding author. Tel.: +44 29 20743512; fax: +44 29 20743500. jamespp{at}cardiff.ac.uk

Objectives The theory of a red blood cell derived nitric oxide (NO) reserve conserving NO bioactivity and delivering NO as a function of oxygen demand has been the subject of much interest. We identified the human coronary circulation as an ideal model system in which to analyse NO metabolites because of its large physiological oxygen gradient. Our objective was to identify whether oxygen drove apportion between various NO metabolite species across a single vascular bed.

Methods Plasma and red blood cell NO metabolites were assessed from the left main coronary artery, coronary sinus and pulmonary artery (providing cross heart and cross pulmonary analysis) of healthy subjects under resting conditions and following administration of an inhibitor of NO biosynthesis. Physiological parameters and angiographic data were monitored throughout the study.

Results Under baseline conditions we observed significant metabolite flux upon the transit of blood across the coronary and pulmonary vascular beds. Whilst there was no net loss of NO through the coronary circulation (p=0.0759), plasma nitrite/protein NO (excluding nitrate) (p=0.0279) and red blood cell sulphanilamide labile signal (p=0.0143) decreased whereas haemoglobin-bound NO increased three-fold (p=0.005). These changes across the coronary circulation were reversed through the pulmonary circuit with red blood cell sulphanilamide labile signal (p=0.0143) and plasma nitrite/protein NO (p=0.0279) increasing and haemoglobin-bound NO decreasing. Blockade of NO synthesis increased mean arterial blood pressure (p<0.01) and reduced coronary artery diameter (p<0.05), however we observed similar apportion of NO metabolites across the heart and lung with no net loss or gain in total NO metabolites.

Conclusions For the first time in human subjects across the resting coronary circulation we reveal significant re-apportionment of NO between metabolite species which correlate with haemoglobin oxygen saturation. These changes occur even within the transit time of blood across this single vascular bed. We demonstrate no net loss/gain of NO from the total metabolite pool across the coronary circulation even where NO biosynthesis is inhibited.

KEYWORDS Nitric Oxide; Metabolites; Coronary; Pulmonary; Flux

1 SCR and AK are joint first authors.


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