In the pig short coronary occlusions induce molecular damage on the pr
otein level in the myocardium, which elicit repair mechanisms by incre
ased transcription and translation, including the activation of potent
ial transcription factors (protooncogenes), genes involved in repair p
rocesses (heat shock genes) or calcium-binding genes. Additionally, so
me growth factors like insulin-like growth factor II show increased tr
anscription in accordance with their function as trophic factors for r
eversibly injured myocardium. Changes in mRNA levels mostly are due to
increased transcription rates and rarely due to prolonged half-life o
f the mRNA. However, at present our data do not allow us to to conclud
e which genes are causative for myocardial stunning and/or ischemic pr
econditioning.