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. Author manuscript; available in PMC: 2015 Oct 4.

Published in final edited form as: Cardiology. 2014 Oct 4;129(3):163–173. doi: 10.1159/000363646

Fig. 1 — Myocardial infarct size after IR. A: Cardiac sections of one representative heart from each group. Isolated hearts from WT and PKO mice were exposed to CON [30-min ischemia and 120-min reperfusion (I-30/R-120)], or IPC [10-min ischemia and 5-min reperfusion (I-10/R-5) plus I-30/R-120] in the absence or presence of rolipram (Ro) (10 μM). After IR, the heart was cut into 5 sections and stained by TTC. Each group contains 6-8 hearts. B: Analysis of infarct size. Infarcted area of myocardium was measured by Image J software. N = 6-8/group. *: p<0.01 vs. CON/WT; #: p<0.01 vs. IPC/WT. †: p<0.01 vs. CON/PKO; §: p<0.01 vs. CON/PKO.

Fig. 1 — Myocardial infarct size after IR. A: Cardiac sections of one representative heart from each group. Isolated hearts from WT and PKO mice were exposed to CON [30-min ischemia and 120-min reperfusion (I-30/R-120)], or IPC [10-min ischemia and 5-min reperfusion (I-10/R-5) plus I-30/R-120] in the absence or presence of rolipram (Ro) (10 μM). After IR, the heart was cut into 5 sections and stained by TTC. Each group contains 6-8 hearts. B: Analysis of infarct size. Infarcted area of myocardium was measured by Image J software. N = 6-8/group. *: p<0.01 vs. CON/WT; #: p<0.01 vs. IPC/WT. †: p<0.01 vs. CON/PKO; §: p<0.01 vs. CON/PKO.