RESEARCH ARTICLE The eNOS 894G/T gene po n

Full list of author information is available at the end of the articleBackground Nitric oxide (NO) is an endothelium-derived relaxing factor (EDRF) which represents one of the most relevant molecules involved in biological systems. NO is synthe-sized by NO Synthase (NOS) from L-arginine. There are three types of NOS: inducible NOS (iNOS), neural NOS (nNOS), and endothelial NOS (eNOS) [1]. The human eNOS gene is located on the chromosome No. 7 (7q35-36) which consists of 26 exons with an entire length of 21 kb and is constitutively expressed in vascular endothelial cells. eNOS is the key enzyme responsible for basal vascular pro-duction of NO [2]. In addition to influencing relaxation of vascular smooth muscle cells, endothelium-derived NO in-hibits platelets [3] and leukocytes [4] adhesion to vascular endothelium, inhibits vascular smooth cell migration and proliferation [5], and limits the oxidation of atherogenic low-density lipoprotein [6]. Furthermore, it has been shown that the production of NO is significantly increased during and after cardiopul-monary bypass (CPB) [7]. The systemic endotoxemia Background: The eNOS 894G/T polymorphism (GG, GT, and TT) is associated with cardiovascular mortality and may influence cardiovascular diseases as a genetic risk factor. Moreover, this polymorphism has an impact on intraoperative hemodynamics during cardiac surgery with cardiopulmonary bypass (CPB). In this study, we analyzed the influence of this gene polymorphism on early clinical outcome in patients who underwent cardiac surgery with CPB. Also, we performed a 5-year follow-up, assessing the impact of this polymorphism on long-term mortality. Method: 500 patients who underwent cardiac surgery with CPB between 2006 and 2007 were included in this prospective single centre study. Genotyping for the eNOS gene polymorphism was performed by polymerase chain reaction amplification