Endothelium, ischemia and the good side of oxygen free radicals.
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.
Grotti
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S
Dipartimento di Medicina Interna, Cardiovascolare e Geriatrica, Università degli Studi di Siena, Siena, Italy.
Gori
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D000975:Antioxidants / Q000378:metabolism; D004730:Endothelium, Vascular / Q000473:pathology*; D005609:Free Radicals; D006801:Humans; D007511:Ischemia / Q000473:pathology*; D019194:Ischemic Preconditioning; D008954:Models, Biological; D008962:Models, Theoretical; D017202:Myocardial Ischemia / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000473:pathology; D009569:Nitric Oxide / Q000737:chemistry; D010100:Oxygen / Q000737:chemistry*; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury; D012307:Risk Factors
D000975:Antioxidants; D005609:Free Radicals; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D010100:Oxygen