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Cardiovascular Research 2005 66(1):7-8; doi:10.1016/j.cardiores.2005.01.022
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Copyright © 2005, European Society of Cardiology

Coronary circulation: Nitric oxide and hypercapnic acidosis

A. Cevese*

Department Neurological Science and Vision. Sect. Physiology, Faculty of Exercise and Sports Science, University of Verona, Via Casorati, 43, 37131 Verona, Italy

* Tel.: +39 45 8952634; fax: +39 45 580881. Email address: antonio.cevese@univr.it

Received 21 January 2005; accepted 27 January 2005

The first 10% of the full text of this article appears below.

See article by Heintz et al. [4] (pages 55–63) in this issue.

In the past two decades, nitric oxide (NO), a molecule whose natural biological role was recognized in a relatively recent period [1], has gained wide credit as a possible agent of physiological and pathological reactions, including those related to the heart and the cardiovascular system. The rapidly increasing wealth of scientific evidence, however, often led to unresolved contradictory results [2], to the extent that, in a recent review on "Nitric oxide and cardiovascular function," Kelly et al. [3] concluded that the explosion of new information over the past 5 years "has generated much light as . . . [Full Text of this Article]


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