THE EFFECT OF DELAYED REPERFUSION FOLLOWING INFARCTION IN THE RAT ON STRUCTURAL-CHANGES IN VIABLE MYOCARDIUM

Objective: Evidence indicates that patency of the infarct related arte ry following the completion of myocardial necrosis can attenuate ventr icular remodeling. Data have also demonstrated that inhibition of infa rct expansion contributes to the anti-remodeling effect of delayed rep erfusion. However, the influence of a patent artery on components of t he remodeling process in the viable myocardium is poorly understood. M ethods: Myocyte morphometrics (isolated cell technique) and collagen c ontent (hydroxyproline analysis) were assessed 28 days following exper imental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperf usion 150 minutes after ligation (RP; n = 11) and a sham-operated grou p (n = 10). Results: Analysis of infarct size (planimetry) in a separa te group of rats demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 +/- 3 vs. RP: 35 +/- 5%). Myocyt e length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 +/- 3 vs. 167 +/- 4 mu m, P = 0.02), in the right ventricle (154 +/- 4 vs. 167 +/- 3 tcm, P = 0.02) and in the septum (158 +/- 4 vs. 169 +/- 4 mu m, p = 0.05). Reperfusion also att enuated the expected increase in cell volume compared with NRP rats (l eft ventricle 39.4 +/- 1.7 x 10(3) vs. 44.1 +/- 1.6 x 10(3) mu m(3), P = 0.06; right ventricle 36.7 +/- 1.6 x 10(3) vs. 42.7 +/- 2.0 x 10(3) mu m(3), p = 0.02; septum 41.0 +/- 1.6 x 10(3) vs. 44.2 +/- 1.8 x 10( 3) mu m(3), p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused grou ps. Conclusion: Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocar dium following infarction in the rat, with no effect on the increase i n collagen content. These data indicate that patency of the infarct ve ssel, 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. (C) 1997 Elsevier Science B.V.