Protein kinase C activation during reperfusion decreases the diastolic stiffness seen in post­ischemic ventricular dysfunction

pp 265-269

Abstract

Experimental evidence suggests that pre-ischemic intra­cellular activation of protein kinase C (PKC) achieves a pro­tective function in ischemic preconditioning. However, the role of PKC during reperfusion remains controversia!. Our airo was to assess whether PKC stimulation during reperfusion would protect the myocardium from post­ischemic dysfunction. We experimentally grouped isolated and isovolumic rabbit hearts by means of 2 different proto­cols. In the first group (Gl, n = 8) hearts were exposed to 15 minutes of global ischemia followed by 30 minutes of reperfusion. The second protocol (G2, n = 8) was similar to G 1 but for the administration of a selective PKC agonist (PMA, 0.2 nM) during the reperfusion phase. Left ventricu­lar developed pressure (LVDP, mm Hg) and end diastolic pressure (LVEDP, mm Hg) (diastolic stiffness) were mea­sured. We found no difference in LVDP between both groups. LVEDP was 39.0 ± 3.2 mm Hg in Gl and 20.9 ± 2.6 in G2 (p< 0.05) after 30 minutes of reperfusion. The infarction size was 2. 7 ± 0.8% in G 1 and 5.0 ± 1.4% in G2 (NS). These findings suggest that PKC stimulation during reperfusion attenuates the increased post-ischemic diastolic stiffness of the ventricle although abnormal contractility and infarction size remain unchanged.