Abstract
The heart is a strictly aerobic body with an energetically very demanding metabolism. Constant supply of oxygen is vital for its normal function.
If the oxygen supply is stopped, such as coronary artery thrombotisation , or severely limited, such as stenosis, myocardial damage occurs due to hypoxia. The amount of hypoxic damage is dependent on the duration of ischemia and also on the resistance to myocardial oxygen deprivation.
This resistance is conditioned by a number of mechanisms at both the biochemical and molecular levels. The aim of this work was to demonstrate UCP2 (-/-) animals resistant to ischemic damage - which we confirmed.
Further evidence of free radical damage at the time and the expression of HIF ischemie. Free radical damage at the time of expression, we have demonstrated