Influence of Intrinsic Aerobic Exercise Capacity and Sex on Cardiac Injury Following Acute Myocardial Ischemia and Reperfusion

Figures

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  Figure 1. Comparison of the percentage of the LV at risk for ischemia (AAR) in the regional ischemia model. The model was reproducible, and the amount myocardium rendered ischemic by coronary occlusion was comparable in all groups.

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  Figure 2. Comparison of the average infarction size normalized to area at risk (%AAR) between HCR male/female and LCR male/female rats after 30 min ischemia and 2 h reperfusion using an in situ regional ischemia (RI) model. Scale bars in images indicate 5 mm. Significant differences were noted between sexes within each phenotype, but not between phenotypes for either sex (*p < 0.05 for the comparison indicated).

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  Figure 3. Comparison of the average infarction size normalized to the whole heart between HCR male/female and LCR male/female rats after 30 min ischemia and 2 h reperfusion using an ex vivo buffer-perfused global ischemia (GI) model. Scale bars in images indicate 5 mm. Significant differences were noted between sexes within each phenotype, but not between phenotypes for either sex (*p < 0.05 for the comparison indicated).

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  Figure 4. Comparison of the average infarction size normalized to area at risk (%AAR) between HCR male/female and LCR male/female rats after 15 min ischemia and 2 h reperfusion using an in situ regional ischemia (RI) model. Infarct sizes were smaller for all groups compared to 30 min regional ischemia (Figure 2). Scale bars in images indicate 5 mm. Significant differences were noted between sexes within each phenotype, and also between phenotypes for each sex, with LCRS having larger average infarctions compared to HCRs (*p < 0.05 for the comparison indicated between sexes within phenotype; **p < 0.05 for the comparison indicated between phenotype within sex).

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  Figure 5. Comparison of the average infarction size normalized to the whole heart between HCR male/female and LCR male/female rats after 15 min ischemia and 2 h reperfusion using an ex vivo buffer-perfused global ischemia (GI) model. Infarct sizes were smaller for all groups compared to 30 min global ischemia (Figure 3). Scale bars in images indicate 5 mm. Significant differences were noted between sexes within each phenotype, and also between phenotypes for each sex, with LCRS having larger average infarctions compared to HCRs (*p < 0.05 for the comparison indicated between sexes within phenotype; **p < 0.05 for the comparison indicated between phenotype within sex).

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  Figure 6. (A) Sample histologic sections showing relative myocardial neutrophil infiltration after 30 min in situ regional ischemia (RI) and 2 h reperfusion by sex and by phenotype in samples from the ischemic region, and from non-ischemic, remote regions (right ventricle) from the same hearts (H&E staining, 60X). Scale bars in images represent 200 um. (B) Quantification of neutrophil infiltration (cell counts). Data represents average of 5 fields in each section, and 5 sections for each animal. Ischemic regions (I) showed higher levels of infiltration compared to non-ischemic remote (NI/R) regions, but the increased levels of infiltration were not different between sexes within either phenotype, and were not different between phenotypes for either sex (*p < 0.05 for the comparison indicated).

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  Figure 7. Summary of arrhythmia scores according to duration of ischemia (30 vs. 15 min), strain (HCR vs. LCR), and sex (males vs. female). There were significant differences in the severity of arrhythmia (*p < 0.05 for the comparison indicated), with 30 min ischemic episode producing consistently higher arrhythmia scores than 15 min events, however there were not significant differences between strain or between sexes with strains.