© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium
Division of Cardiovascular Medicine, Department of Medicine, University of Minnesota, Box 508 UMHC, 420 Delaware Street SE, Minneapolis, MN 55455, USA
* Corresponding author. Tel.: (+1-612) 6257924; Fax: (+1-612) 6264411; E-mail: mcdon003@maroon.tc.umn.edu
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 µm, p = 0.02), in the right ventricle (154±4 vs. 167±3 µm, p = 0.02) and in the septum (158±4 vs. 169±4 µm, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4±1.7x103 vs. 44.1±1.6x103 µm3, p = 0.06; right ventricle 36.7±1.6x103 vs. 42.7±2.0x103 µm3, p = 0.02; septum 41.0±1.6x103 vs. 44.2±1.8x103 µm3, 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.
KEYWORDS Myocyte hypertrophy; Rat myocardial infarction; Reperfusion; Collagen; Ventricular remodeling
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