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Issue title: Selected Proceedings of the 14th European Conference for Clinical Hemorheology and Microcirculation, Dresden, Germany, June 27–30, 2007
Article type: Research Article
Authors: Grotti, S. | Gori, T.
Affiliations: Dipartimento di Medicina Interna, Cardiovascolare e Geriatrica, Università degli Studi di Siena, Siena, Italy
Note: [] Corresponding author: Tommaso Gori, MD, PhD, Dipartimento di Medicina Interna, Cardiovascolare e Geriatrica, Università degli Studi di Siena, 53100 Siena, Italy. Tel.: +39 0577 585350; Fax: +39 0577 233318; E-mail: tommaso.gori@ utoronto.ca.
Abstract: Pathophysiological studies have clearly demonstrated that the relationship between endothelial (dys)function and tissue ischemia is bidirectional: while it is well accepted that endothelial dysfunction has a key role in the progression and the instabilization of coronary atherosclerosis, it is also well known that the endothelium is particularly sensitive to ischemia and reperfusion injury, and that this damage is an important component in determining the size of the infarction. Therefore, protecting the endothelium from ischemia has potentially important clinical implications. In this scenario, a particularly important role is played by reactive oxygen species: these elusive mediators are involved in determining the endothelial toxic effect of risk factors, are involved in reperfusion injury, but, most importantly, also have a role in endothelial preconditioning, a protective process that is characterized by a reduced sensitivity to ischemia and reperfusion. The present paper reports considerations regarding these phenomena as discussed in a lecture at the recent Conference of the European Society of Clinical Hemorheology and Microcirculation held in Dresden, Germany.
Keywords: Oxygen free radicals, ischemia, reperfusion, endothelium, endothelial dysfunction, nitric oxide, ischemic preconditioning
DOI: 10.3233/CH-2008-1082
Journal: Clinical Hemorheology and Microcirculation, vol. 39, no. 1-4, pp. 197-203, 2008
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