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The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium
1Department of Medicine, University of Minnesota, Minneapolis 55455, USA. mcdon003@maroon.tc.umn.edu
Insights
Delayed reperfusion following myocardial infarction, even without saving heart muscle, reduces myocyte enlargement. This indicates that keeping the infarct artery open has anti-remodeling effects beyond the infarct zone.
Area of Science:
- Cardiovascular Research
- Myocardial Infarction
- Cardiac Remodeling
Background:
- Patency of the infarct-related artery after myocardial necrosis can limit ventricular remodeling.
- Delayed reperfusion's anti-remodeling effect is partly due to inhibiting infarct expansion.
- The impact of a patent artery on viable myocardium during remodeling is not well understood.
Purpose of the Study:
- To investigate the effect of reperfusion on myocyte size and collagen content in viable myocardium following experimental myocardial infarction.
- To determine if late reperfusion, without reducing infarct size, influences cardiac remodeling in non-infarcted areas.
Main Methods:
- Experimental myocardial infarction was induced in rats.
- Rats were divided into permanently ligated (NRP) and reperfused (RP) groups 150 minutes post-ligation.
- Myocyte morphometrics and collagen content (hydroxyproline) were assessed 28 days post-infarction.
Main Results:
- Late reperfusion did not reduce infarct size.
- Reperfusion significantly attenuated myocyte length and volume increases in viable left ventricle, right ventricle, and septum.
- Collagen content increased in viable left ventricular tissue in both reperfused and non-reperfused groups.
Conclusions:
- Reperfusion without myocardial salvage mitigates myocyte hypertrophy and volume changes in remodeling myocardium.
- Patency of the infarct artery exerts an anti-remodeling effect in areas remote from the infarct zone.
- These findings suggest that maintaining infarct artery patency is beneficial for limiting adverse cardiac remodeling.
Objective:
Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood.
Methods:
Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham-operated group (n = 10).
Results:
Analysis of infarct size (planimetry) in a separate group of rats demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 +/- 3 vs. RP: 35 +/- 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 +/- 3 vs. 167 +/- 4 microns, p = 0.02), in the right ventricle (154 +/- 4 vs. 167 +/- 3 microns, p = 0.02) and in the septum (158 +/- 4 vs. 169 +/- 4 microns, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 +/- 1.7 x 10(3) vs. 44.1 +/- 1.6 x 10(3) micron 3, p = 0.06; right ventricle 36.7 +/- 1.6 x 10(3) vs. 42.7 +/- 2.0 x 10(3) micron 3, p = 0.02; septum 41.0 +/- 1.6 x 10(3) vs. 44.2 +/- 1.8 x 10(3) micron 3, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups.
Conclusion:
Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti-remodeling effect remote from the area perfused by this artery.