Analytica Chimica Acta 505 (2004) 115–123 Possible mechanism for nitric oxide and oxidative stress induced pathophysiological variance in acute myocardial infarction development A study by a flow injection–chemiluminescence method Dachun Yao a , Athanasios G. Vlessidis a , Nicholaos P. Evmiridis a,∗ , Stavros Siminelakis b , Niokou Dimitra c a Laboratory of Analytical Chemistry, Department of Chemistry, University of Ioannina, 45110 Ioannina, Greece b Department of Cardiothoracic Surgery, University Hospital of Ioannina, 45110 Ioannina, Greece c Department of Anesthesiology, University Hospital of Ioannina, 45110 Ioannina, Greece Received 9 July 2002; received in revised form 1 October 2002; accepted 21 November 2002 Abstract The acute myocardial infarction (AMI) model was established through rabbits, and this kind of model was used to investigate the possible mechanism for the AMI mediated damage, induced by NO release and oxidative stress. The biomedical parameters nitric oxide (NO), total antioxidant capacity (TAC) variation in vivo and the enzymatic activity of nitric oxide synthase (NOS) and superoxide dismutase (SOD), which are considered as the major markers for pathophysiological variation, were detected. The results obtained gave evidence that AMI can lead to the NO excess release and compensation by excess cellular respiration, and both of them can result in oxidative stress and further generation of reactive oxygen species (ROS). The latter can bring a series of damages to the organism, including decrease of the TAC value, and NOS and SOD activity. © 2002 Elsevier Science B.V. All rights reserved. Keywords: Acute myocardial infarction; Nitric oxide; Total antioxidant activity; Nitric oxide synthase; Superoxide dismutase; Chemiluminescence; Flow injection 1. Introduction Acute myocardial infarction (AMI) is muscle cell necrosis due to vessel obstruction (coronary artery occlusion); the cell is damaged because the oxygen supply to the cell mitochon- dria is dropped abruptly. During reperfusion (after a heart operation) or the release of vessel occlusion in experimen- tal modules, the reactive oxygen species (ROS) in the blood causes further cell damage due to oxidative stress (distur- bance in the prooxidant–antioxidant balance in favor of the former [1]) brought about by the ROS of the incoming blood. Acute myocardial infarction is one kind of serious dis- ease that can bring much damage to the human being. In an acute myocardial infarction, a series of related pathological ∗ Corresponding author. Tel.: +30-26510-98702; fax: +30-26510-44831. E-mail address: nevmirid@cc.uoi.gr (N.P. Evmiridis). responses is taking place. It is quite important to obtain a sound understanding of the biochemistry involved in vivo that results in the pathological states of organisms in order to achieve a reasonable treatment plan for the favorable prog- nosis or successful medical treatment of the damage [2–4]. It is well known that nitric oxide (NO) plays an important role for maintaining vascular homeostasis [5–7]. Further- more, according to the literature, NO as a free radical may bring further damage and generation of ROS; NO also is considered as a potential antioxidant [8–11]. Up to now, the exact role of NO in AMI is unclear since NO has very short half-life in vivo, and it is hard to achieve an accurate measurement [12]. As a unique enzyme that can generate NO in vivo un- der physiological conditions, nitric oxide synthase (NOS) has three different isoforms, which are isolated and purified from cells of different organs. eNOS comes from endothe- lial cells, nNOS or bNOS comes from a neuron system such 0003-2670/$ – see front matter © 2002 Elsevier Science B.V. All rights reserved. doi:10.1016/S0003-2670(02)01536-2