Postconditioning attenuates coronary perivascular and interstitial fibrosis through modulating angiotensin II receptors and ACE2 following myocardial infarction

Abstract Background Postconditioning (Postcon) is known to reduce infarct size. This study tested the hypothesis that Postcon attenuates the perivascular and interstitial fibrosis after myocardial infarction through modulating angiotensin II-activated fibrotic cascade. Materials and methods Male Sprague-Dawley rats were subjected to 45 min coronary occlusion followed by 1 and 6 weeks of reperfusion. Postcon was applied at the onset of reperfusion with 4 cycles of 10/10s reperfusion/ischemia at the onset of reperfusion. Preconditioning (Precon) with 2 cycles of 5/5min ischemia/reperfusion was applied before coronary occlusion. Results Postcon reduced ACE protein and expression in the perivascular area and intermyocardium, coincident with the less-expressed AT1 receptor, enhanced AT2 receptor and ACE2. Postcon lowered the MCP-1 protein and inhibited the populations of interstitial macrophages (60±12 vs. 84±9.5 number/HPF in control, p