AMP-activated protein kinase mediates ischemic glucose uptake and prevents postischemic cardiac dysfunction, apoptosis, and injury
J. Clin. Invest. Raymond R. Russell, et al. 114:495 doi:10.1172/JCI19297 [
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Figure 7Myocardial injury and apoptotic activity following low-flow ischemia. Release of myocardial creatine kinase (CK) and lactate dehydrogenase (LDH) from WT (
n = 7) and KD (
n = 6) transgenic hearts during ischemia and reperfusion (
A and
B). Caspase-3 activity following baseline perfusion (
n = 3 for both groups) and following ischemia/reperfusion (
n = 7 for WT and
n = 6 for KD) (
C). Quantification of apoptotic nuclei from WT and KD hearts (
n = 3 for both) following ischemia/reperfusion (
D). Representative composite confocal photomicrographs of sections from WT and KD hearts following reperfusion (
E and
F). Hearts underwent TUNEL staining with fluorescein-labeled dUTP and counterstaining with propidium iodide. TUNEL-positive nuclei are stained yellow (arrows). *
P < 0.05 versus WT;
P < 0.05 versus ischemia;
†P < 0.05 versus baseline.
