α-MHC-tTA hearts were protected against I/R injury <i>in vitro</i> using the Langendorff-perfused heart.

<p>(A–B) LVDP was similar between α-MHC-tTA and control hearts at baseline; however, after 30 min of ischemia, control hearts recovered to 35% of baseline LVDP values whereas α-MHC-tTA had 90% recovery. (C–D) LV systolic and diastolic functions assessed by dP/dt_max and dP/dt_min respectively were significantly higher in α-MHC-tTA compared to control after 30 min of ischemia. (N = 3 for control and N = 4 for αMHC-tTA, p<0.05).</p

Echocardiographic Measurements and Heart weight/tibia length.

<p>Values are mean ± SEM. <i>P</i> values are based on 1-tail Student's <i>t</i>-test assuming unequal variance.</p

Reduced cardiac muscle damage in α-MHC-tTA hearts subjected to I/R injury.

<p>Lack of cardiac muscle cell damage was apparent in α-MHC-tTA compared to control where abundant creatine kinase levels were observed within 15 min of start of reperfusion. (N = 4, p<0.05).</p

Effect of <i>in vivo</i> I/R injury on α-MHC-tTA hearts.

<p>Significantly smaller infarct sizes were observed in α-MHC-tTA hearts subjected to 45 min of left coronary artery occlusion followed by 120 min of reperfusion. (A) Representative cross sections from control and α-MHC-tTA hearts. (B) Average infarct size in control and α-MHC-tTA hearts. (N = 5 for control and N = 7 for α-MHC-tTA, p<0.05).</p

Effect of PI3K inhibition on the protection against I/R injur in α-MHC-tTA hearts.

<p>Administration of LY294002 did not abolish the protective effect seen in α-MHC-tTA hearts however it did abolish protection imparted by IPC. (N = 5 for α-MHC-tTA and N = 3 for α-MHC-tTA+8 µM LY294002, p<0.05).</p