Non-elastic deformation of myocardium in low-flow ischemia and reperfusion: Ultrastructure-function relations

This study tested the hypothesis that regional low-flow ischemia and reperf usion alter myocardial material properties by causing non-elastic deformati on. Twenty-two anesthetized, open-chest pigs were studied, Pigs underwent 9 0 min of regional low-now ischemia (anterior LV subendocardial blood flow 2 9 +/- 7% of baseline) followed by 90 min reperfusion. LV pressure and regio nal subendocardial segment length were recorded to derive end-diastolic pre ssure vs segment length (EDP vs EDL) and preload-recruitable stroke work (P RSW) relations. In vivo, non-elastic myocardial deformation was inferred fr om increases in minimally loaded myocardial dimensions: the EDL at zero EDP (Ln) and the EDL at which no regional external work was performed (L-w, th e PRSW intercept), In 15 pigs, ultrastructural confirmation of non-elastic deformation was obtained from sarcomere dimensions measured by transmission electron microscopy after in situ perfusion fixation under non-ischemic co nditions, after 90 min ischemia, or after 90 min ischemia plus 90 min reper fusion. Ischemia increased L-0 and L-w to 1.17+/-0.05 and 1.13+/-0.04 times baseline, respectively, After reperfusion, L-0 and L-w remained increased to 1.09 +/- 0.03 and 1.15+/-0.02 times baseline (all P<0.05), After reperfu sion, PRSW slope was not different from baseline, but regional external wor k remained depressed (0.38 +/- 0.03 times baseline) due to the persistent i ncrease in L-w, Neither L-0 nor L-w changed in the posterior (non-ischemic) region. In hearts fu;ed after ischemia or after ischemia plus reperfusion, sarcomere length was significantly greater and transverse distance between thick myofilaments was significantly smaller in the anterior (ischemic) su bendocardium than in the posterior (non-ischemic) subendocardium (P<0.01). We conclude that regional low-flow ischemia and reperfusion cause non-elast ic deformation of myocardium, manifest in vivo by increased minimally loade d myocardial dimensions (L-0 and L-w) and ultrastructurally by increased sa rcomere length and decreased transverse interfilament distance, Non-elastic deformation of myocardium may contribute to contractile dysfunction in low -flow ischemia and reperfusion. (C) 1999 Academic Press.