EFFECTS OF ISCHEMIC POSTCONDITIONING ON REPERFUSION INJURY IN

JC FANTINELLI; SM MOSCA

Buenos Aires, Argentina

Congreso; XI Congreso Argentino de Hipertensión Arterial; 2004

It has been shown recently that brief intermittent ischemia applied during the onset of reperfusion (¨ischemic postconditioning¨: IPC) reduces myocardial injury in normotensive animals. To determine the effect of IPC on myocardial stunning in hypertensive rats, isolated hearts from SHR of 6 months of age with arterial pressure values of 185 ± 5 mmHg were submitted to the following protocols: I) Control: 20 min of stabilization period, 20 min of normothermic global ischemia (GI) and 30 min of reperfusion (R); II) PCI: 20 min of stabilization period, 20 min of GI, 5 min of R, 5 min of GI and 20 min of R. Systolic function was assessed by left ventricular developed pressure (LVDP) and +dP/dtmax and diastolic function by left ventricular end diastolic pressure (LVEDP). To examine IPC action on ROS-induced damage of myocardium, lipid peroxidation was assessed by determining thiobarbituric acid-reactive substances (TBARS). In control group, at the end of R, LVDP and +dP/dtmax reached values of 47 ± 9 % and 46± 9 % of preischemic values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. ventricular end diastolic pressure (LVEDP). To examine IPC action on ROS-induced damage of myocardium, lipid peroxidation was assessed by determining thiobarbituric acid-reactive substances (TBARS). In control group, at the end of R, LVDP and +dP/dtmax reached values of 47 ± 9 % and 46± 9 % of preischemic values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. ventricular end diastolic pressure (LVEDP). To examine IPC action on ROS-induced damage of myocardium, lipid peroxidation was assessed by determining thiobarbituric acid-reactive substances (TBARS). In control group, at the end of R, LVDP and +dP/dtmax reached values of 47 ± 9 % and 46± 9 % of preischemic values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. values, respectively. LVEDP increased from 10 ± 1 to 53 ± 8 mmHg at 30 min of R. IPC improved significantly postischemic recovery of contractility (LVDP =95 ± 8 %; +dP/dtmax = 92 ± 8 %) and decreased myocardial stiffness (LVEDP at the end of R = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to ischemia-reperfusion and attenuates lipid peroxidation. These data suggest that diminution of ROS attack to cardiac membranes may be the mechanism responsible of cardioprotection by IPC. = 27 ± 7 mmHg). TBARS diminished significantly in postconditioned rats (5.86 ± 0.85 vs 12.80 ± 0.23 nmol/g in control hearts). In conclusion, ischemic postconditioning confers protection to the SHR myocardium against systolic and diastolic dysfunction following to is