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Cardiovascular Research 1999 44(3):474-476; doi:10.1016/S0008-6363(99)00367-3
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Oxidative stress, F2-isoprostanes and endothelial dysfunction in hypercholesterolemia

Carlo Palomboa,b,*, Valter Lubranoa,c and Tiziana Sampietroa

aCNR Institute of Clinical Physiology, University of Pisa, Via Roma 67, 56126 Pisa, Italy
bDepartment of Internal Medicine, University of Pisa, Via Roma 67, 56126 Pisa, Italy
cDepartment of Oncology, Division of Pharmacology, University of Pisa, Via Roma 67, 56126 Pisa, Italy

* Corresponding author. Tel.: +39-50-583-288; fax: +39-50-553-461 palombo@po.ifc.pi.cnr.it

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

See article by Wilson et al. [9] (pages 601–607) in this issue.


   1 Introduction
 
Hypercholesterolemia is reported to be associated both with enhanced oxidative stress, related to increased lipid peroxidation [1], and with augmented susceptibility to coronary vasoconstriction [2]. The abnormal coronary vasoreactivity is mainly attributed to endothelial dysfunction, which in hypercholesterolemic man has been demonstrated by several approaches, including coronary and forearm blood flow response to acetylcholine (ACh) [3,4], and flow-mediated dilation [5]. An increased generation of oxidized LDL is a major factor responsible for the vascular damage related to high cholesterol levels, and oxidative stress leads to increased breakdown and/or reduced bioavailability of NO in a number of experimental and clinical models [6]. F2-Isoprostanes, namely 8-epi-prostaglandin F2{alpha} (8-epi-PGF2{alpha}), have been recently proposed as . . . [Full Text of this Article]


   2 Hypercholesterolemia and oxidative stress
 

   3 Endothelial dysfunction and coronary tone
 

   4 The double facet of F2-isoprostanes: markers of oxidative stress and modulators of coronary tone
 

   5 Conclusions
 

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