Possible mechanism for nitric oxide and oxidative stress induced pathophysiological variance in acute myocardial infarction development, A study by a flow injection–chemiluminescence method

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.