Effects of Renal Ischemic Postconditioning on Myocardial Ultrastructural Organization and Myocardial Expression of Bcl-2Bax in Rabbits

Abstract EN

We investigated the cardioprotective effect of renal ischemic postconditioning (RI-PostC) and its mechanisms in a rabbit model.

Rabbits underwent 60 min of left anterior descending coronary artery occlusion (LADO) and 6 h of reperfusion.

The ischemia-reperfusion (IR) group underwent LADO and reperfusion only.

In the RI-PostC group, the left renal artery underwent 3 cycles of occlusion for 30 seconds and release for 30 seconds, before the coronary artery was reperfused.

In the RI-PostC + GF109203X group, the rabbits received 0.05 mg/kg GF109203X (protein kinase C inhibitor) intravenously for 10 min followed by RI-PostC.

Light microscopy and electron microscopy demonstrated that the RI-PostC group showed less pronounced changes, a smaller infarct region, and less apoptosis than the other two groups.

Bcl-2 and Bax protein expression did not differ between the IR and RI-PostC + GF109203X groups.

However, in the RI-PostC group, Bcl-2 protein expression was significantly higher and Bax protein expression was significantly lower than in the other two groups (P<0.05).

Changes in heart rate and mean arterial pressure were also smaller in the RI-PostC group than in the other two groups.

These results indicate that RI-PostC can ameliorate myocardial ischemia-reperfusion injury and increase the Bcl-2/Bax ratio through a mechanism involving protein kinase C.