Comparative effects of ischemic pre and postconditioning on ischemia-reperfusion injury in spontaneously hypertensive rats (SHR).

FANTINELLI, JC; MOSCA, SM

MOLECULAR AND CELLULAR BIOCHEMISTRY

Springer Link

Año: 2007 vol. 296 p. 45 - 51

0300-8177

Brief episodes of myocardial ischemia-reperfusion applied early in reperfusion may attenuate the reperfusion injury, strategy called ischemic postconditioning (IPO). Our objective was to examine the effects of IPO compared with ischemic preconditioning (IP) on postischemic myocardial dysfunction in spontaneously hypertensive rats (SHR). Isolated hearts from SHR and normotensive WKY rats were subjected to the following protocols: 1) Ischemic control (IC): global ischemia 20 min (GI20) and reperfusion 30 min (R). 2) IPO: three cycles of R30sec-IG30sec at the onset of R; 3) IP: a cycle of IG5-R10 previous to GI20, 4) IPO in the presence of chelerythrine, an inhibitor of protein kinase C (PKC). Systolic and diastolic function were assessed through developed pressure (LVDP) and end diastolic pressure (LVEDP), respectively. Lipid peroxidation was estimated by thiobarbituric reactive substance (TBARS) concentration. IPO significantly improved postischemic dysfunction. At the end of R, LVDP recovered to 87 ± 7 % in WKY and 94 ± 7 % in SHR vs 55 ± 11 % and 58 ± 12 % in IC hearts. LVEDP reached values of 24 ± 6 mmHg for WKY and 24 ± 3 mmHg for SHR vs 40 ± 8 and 42 ± 5 mmHg in IC hearts. Similar protection was achieved by IP. TBARS contents of SHR hearts were significantly diminished by IP and IPO. PKC inhibition aborted the protection of myocardial function and attenuated the diminution of lipid peroxidation conferred by IPO. These data show that IPO was as effective as IP in improving the postischemic dysfunction of hearts from SHR hearts, and that this cardioprotection appears to be associated with a diminution of ROS-induced damage involving the PKC activation.