Effects of oxidative stress on vascular function, and the role of anesthetics

Excerpt

H. Kinoshita The roles of reactive oxygen species and oxidative stress continue to be an area of interest in vascular biology and pathology [1]. Oxidative stress can be defined as imbalance between reactive oxygen species and antioxidants (Fig. 1). Oxygen-derived free radicals, including superoxide and hydroxyl radicals, are a subgroup of reactive oxygen species containing one or more unpaired electrons [2]. Superoxide, which is generated from molecular oxygen, is a precursor of several reactive oxygen species and, therefore, it seems necessary to reveal its role in oxidative stress of the vasculature. Previous studies demonstrated multiple sources of superoxide within vascular endothelial and smooth muscle cells, including mitochondria, cyclooxygenase, NADPH oxidase, xanthine oxidase, lipoxygenase, and dysfunctional nitric oxide synthase [2, 3]. Among these, NADPH oxidase is known to be a crucial system for superoxide production in vascular pathology [3, 4]. The vascular NADPH oxidases include the NOX1, NOX2, NOX4, and NOX5 subtypes [5]. NOX1 and NOX2 subtypes are particularly important sources of superoxide production within the vascular wall in many diseased states, including hypertension, diabetes mellitus, inflammation, metabolic syndrome, and heart failure [6‐9].

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