Objectives To observed the protective effects of Renal sympathetic denervation (RSD) on myocardial interstitial remodelling, By detected the expression level of MMP-2,9 in infarcted border zone (IBZ), myocardial infarcted zone (MIZ) and noninfarcted zone (NIZ) of myocardium.
Methods The left anterior descending coronary artery of canine was embolismed by gelatin sponge through cardiac catheter to produce a post-myocardial infarction heart failure model. Canine were randomly divided into the groups of controls (G0) and experiments (G1-3). All groups do the embolismed, and experimental group do the RSD 4 weeks after the infarction. Animals in G1-3 were executed at 2, 3 and 4 weeks after RSD operation respectively, the myocardial specimens were taken to assess. Immunohistochemistry method was used to examine the expression of MMP-2,9.
Results The amount of MMP-2 increased significantly at 3 days after infarction and reached its peak at 4 weeks, then develops the tendency to declines and finally stabilised at 6 to 8 weeks after embolismed. There was a similar trend of change in MMP-9. Its concentration was not increase significantly until 1 week after MI, peak soon then shown a downward trend and stabilised at 8 weeks. MMP-2,9 is distributed mainly over infarcted zone>infarcted border zone>noninfarcted zone of myocardium.
Conclusions Embolisming coronary artery by gelatin sponge is mini-invasive interventional method to produce a post-myocardial infarction heart failure model, could be applied wildly because its safeness and trustiness. MMP-2,9 was distributed mainly in infarcted zone over than infarcted border zone, while Renal sympathetic denervation can reduced the expression in myocardium as time passed. One possible explanation of the cardiac function protective effect on post-myocardial infarction heart failure model from RSD that is RSD inhibit MMP-2,9 expression to impact the myocardial interstitial remodeling.
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