title: Reactive oxygen and nitrogen species: implications for cardiovascular device engineering.
abstract: The development of medical devices for cardiovascular applications has suffered due to lack of understanding of why vascular wall cells act nonphysiologically when exposed to biomaterials. One possible reason might be the chemical environment associated with cardiovascular disease. An improved understanding of cellular and subcellular mechanisms may assist in future device design to account for the disease environment. Reactive oxygen and nitrogen species (ROS/RNS) are produced through normal cellular metabolism and are rendered harmless by enzymatic systems. However, during a disease process, these systems may act aberrantly, and either fail to convert ROS and RNS to harmless substances or by producing more oxidants. There is indirect evidence that the implantation of biomedical materials may also be responsible for the triggering of these aberrant pathways that may lead to the eventual failure of the device. The understanding of how the vascular environment may be changed at the subcellular level by the presence of a biomaterial is critical. In the following pages, we hope to review the current thinking within vascular biology regarding ROS and RNS, how they are measured, and how they may impact vascular cells.
authors: Cell and Synthetic Interface Engineering Laboratory, Department of Biomedical Engineering, The University of Iowa, Iowa City, Iowa 52242, USA. kkader@engineering.uiowa.edu
authors: Khalid N
authors: KN
authors: Kader
authors: Christian H
authors: CH
authors: Coyle
mesh_terms: D000818:Animals; D002319:Cardiovascular System; D006801:Humans; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D019736:Prostheses and Implants; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D016877:Oxidants; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species