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J Thorac Cardiovasc Surg 2001;122:821-822
© 2001 The American Association for Thoracic Surgery
Brief Communications |
From the Service des Explorations Fonctionnelles Respiratoires et Circulatoiresa and Service de Chirurgie Cardiovasculaire,b Hôpitaux Universitaires, Strasbourg, France.
This work was supported by grants of the Faculty of Médicine, Louis Pasteur University, and the Strasbourg University Hospital, Strasbourg, France.
Received for publication Feb 2, 2001. Accepted for publication Feb 5, 2001. Address for reprints: Bernard Geny, Institut de Physiologie, Faculté de Médecine, 67085 Strasbourg Cedex, France (E-mail: Bernard.Geny@]physio-ulp.u-strasbg.fr).
Despite subjective functional improvement and improvement in quality of life, heart transplant recipients demonstrate a persistent reduction in exercise capacity. Central factors, such as cardiac dysfunction and chronotropic insufficiency, likely participate in this limitation, but numerous studies underlined the role of peripheral factors.
1 Nitric oxide (NO), mainly produced in the endothelium, is a major component involved in both basal and exercise vascular tone, and flow-mediated release of NO is thought to be important for exercise-induced vasodilation. Interestingly, an exercise-induced increase in circulating nitrates and nitrites (NOx), the stable end product reflecting NO production, has recently been observed and was associated with physical fitness in healthy human subjects.
2,3 Furthermore, supplementation with the NO precursor L-arginine enhanced endothelium-dependant vasodilation and exercise capacity in patients with heart failure.
4 We therefore investigated whether impaired NO release might participate in exercise limitation after heart transplantation.
Method and results
Plasma NOx values were determined by the colorimetric method on the basis of the Griess reaction before, at 70% of peak, at peak, and at 10, 30, and 60 minutes of recovery during a
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