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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


ROLE OF UNCOUPLING PROTEINS IN HEART FUNCTION CHANGES DURING ISCHAEMIA-REPERFUSION
Abstract number: OTH13-50

Sagach1 V.F., Shymanskaya1 T.V., Dobrovolsky1 F.V., Goshovska1 Y.V.

1Circulation Physiology Department, Bogomoletz Physiology Institute of NAS, Kyiv, Ukraine; [email protected]

Aim: 

Heart ischaemia is well-known damaging agent, which is more evidently performed via mitochondria. Uncoupling proteins (namely UCP2 and UCP3) are the members of inner membrane transporters family that dissipating the proton gradient. Ischaemic injury and UCPs appear to be interrelated. In this study we hypothesized that UCPs are involved in pathological processes occurred in cardiac cells during ischaemia.

Methods: 

In experiments on isolated rat hearts perfused under Langendorff preparation effects of ischaemia-reperfusion and blockade of UCPs with its inhibitor genipin (50 mg/L) was studied and cardiodynamic parameters were measured. Expression of UCPs was detected by reverse transcriptional polymerase chain reaction.

Results: 

It was shown that postischaemic disturbances of cardiac contractility, coronary vessels tone and heart rate are accompanied with noneffective oxygen utilization by myocardial tissue. At the same time ischaemia (20 min) as well as subsequent reperfusion (40 min) increased expression of UCPs in myocardium: mRNA levels of UCP3 were significantly higher that those of UCP2, but both higher that in control. Blockade of UCPs by genipin has, in general, positive effect: increased indexes of cardiac contractility decreased oxygen cost of myocardial work and improved non-effective oxygen utilization by the heart tissue during perfusion. However, postischaemic heart disturbances after genipin administration were higher than in control.

Conclusions: 

Our results demonstrate that UCPs seem to play regulatory role in cardiac activity during ischaemia-reperfusion. We suggest that uncoupling proteins (UCP2 and UCP3) are implicated in pathological mechanisms developed during ischaemia-reperfusion.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :OTH13-50

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