The development of ischemic heart disease results from a decreased blood flow through the myocardium, usually caused by arteriosclerosis. The myocardium suffers from ischemia (insufficient blood supply) and consequently, insufficient oxygen supply. The end stage is then infarction (heart attack).
In order to improve the treatment of ischemic heart disease and thus the prevention of heart attack, we study the mechanisms that play a role in the resistance of myocardium to the damage caused by hypoxia (oxygen deprivation). We investigate an increased myocardial resistance to ischemia, both innate at neonatal heart and artificially induced. There are 2 ways how to stimulate the myocardial resistance to ischemia – either adaptation to chronic hypoxia or physical exercise. On contrary, we also study animal models with pathologically enhanced sensitivity to ischemic damage due to the presence of various forms of systemic hypertension and dyslipidaemia (increased levels of lipids or lipoproteins in the blood plasma).
Studying an isolated perfused rat heart, we can monitor perfusion (flow) through myocardial blood vessels and estimate histochemically the size of area of infarction.
Physical exercise represents a way how to stimulate the resistance of heart to ischemia. Rats are running on a threadmill.