Background: Protein phosphorylation plays a very important role in the modulation of signal transduction in many tissues including heart. The activities of protein tyrosine kinases (PTKs) of the heart are rather low but PTKs in cardiac myocytes could be involved in many processes including necrosis, apoptosis, and inflammation. All of them lead to heart failure and are the result of such conditions as ischemia and reperfusion. The aim of our study was to investigate if the ischemia and reperfusion could change the protein tyrosine kinases activities in rat cardiac myocytes.
Material and methods: The specific activities of PTKs were defined as 32P incorporation into exogenous poly (Glu, Tyr) – known as an artificial substrate for all types of protein tyrosine kinases.
Results: The activity of tyrosine kinases in ischemic heart was lower than in control-intact heart and amounted to 50-60% of control values. In the heart after ischemia and following reperfusion the activities of PTKs increased to 135% of control.
Conclusion: Ischemia and reperfusion changed activity of PTKs. There were no differences in protein tyrosine activity between the left and right ventricles.

Keywords: protein tyrosine kinases, Rat heart, Ischemia, Reperfusion