Investigation of the Oxidative Stress, the Altered Function of Platelets and Neutrophils, in thePatients with Peripheral Arterial Disease

Ischemia reperfusion injury (I/R) is a relevant problem in case of myocardial infarction (Moens AL, Claeys MJ et al. 2005.), stroke, (Kato H and Kogure K 1999), coronary bypass surgery, (Bakkaloglu C, and Soyagir B, 2006), under thrombolysis, (Krumholz HM and Goldberger 2006), revascularization surgery of lower limb (Arato et al 2006., Laird IR 2003), balloon angioplasty (Weissand A.G. and Zahger AT 1999) and in every cases, when the physiological blood flow in the occluded vessels are restored (Falkensammer J and Oldenburg WA 2006), (Ferencz A et al 2004). Vessel closure and hypoxia can be caused by embolism (thrombus, tumour, fat, foreign body) stenotic arteriopathy, arterial spasm, compression, arterial thrombus, trauma, etc. During the exclusion of a segment of the vessels from the circulation, ischemia and acidosis appeared in the surrounding tissues. In case of the heart, when oxygen supply is inadequate, the respiration shift from aerobic fatty acid consumption and metabolism to anaerobic glycolysis, resulting in a reduced ATP production. The results of hypoxia in the metabolically active tissues (cardiac, skeletal muscle and neuronal tissues) are more profound than in other cell types. The cells are exposed to hypoxia try to adapt to the absence of oxygen, by switching their metabolism from aerobic to anaerobic. Finally this strategy leads to tissue damages and loss of cells too, as it can be seen in acute or chronic occlusive diseases, as well. The measures of the tissue injuries depend on the duration of hypoxia, the mass of tissues are involved, the ATP requirement of the cell types and the blood pressure of the patients. Under hypoxic condition the generations of reactive oxygen species (ROS), such as O2.-, H2O2, are increased. During normoxyc, physiological condition mitochondria generate low level of ROS by the respiratory chain. These are managed by natural antioxidants, such as manganese superoxid dismutase (SOD) in the mitochondria, or copper-zinc SOD in the inter-membrane space in the mitochondria, and in the cytosol, making the dismutation of superoxide anion