Introduction (3)

Although studies of animal models to modify the outcome of MIRI showed promising results, the number of human studies is limited, and results thus far are disappointing. The basis for the apparent discrepancy between animal and human studies is unclear and may include species differences in mechanisms underlying MIRI or differences in organ sensitivity towards MIRI. Animal experiments are generally performed in young and healthy animals.

This obviously contrasts to the human population exposed to MIRI indicating pitfalls in the interpretation of animal models in such a convoluted process as MIRI.

We now propose a new clinical model to obtain information about the underlying mechanisms of MIRI by measuring various established markers for each of these processes in paired arterial and venous (coronary sinus) samples. We assess the contribution of oxidative damage, complement, endothelial, thrombocyt and neutrophil activation and inflammation to human MIRI. Obtained data will provide information to understand MIRI, its possible contribution to SIRS and may provide for the development of a rational prevention or treatment strategy leading to a decline in morbidity and mortality rates.