Loss of elastic recoil in postischemic myocardium induces rightward shift of the systolic pressure-volume relationship
Krams, R.; Janssen, M.; Van der Lee, C.; Van Meegen, J.; De Jong, J.W.; Slager, C.J.; Verdouw, P.D.
American Journal of Physiology 267(4 Pt 2): H1557-H1564
1994
ISSN/ISBN: 0002-9513 PMID: 7943402 Document Number: 430584
Ischemia-induced systolic dysfunction has been ascribed to changes in cellular excitation-contraction coupling and diastolic dysfunction because of disruption of the extracellular collagen matrix. Therefore, systolic and diastolic pressure-volume relationships and O2 consumption were determined before and after 5 min of global ischemia in isolated blood-perfused porcine hearts. The slope of the systolic pressure-volume relationship was 7.2 ± 0.6 (SE) mmHg ml-1 100 g-1 (n = 18) at baseline and did not change during reperfusion, but the systolic volume intercept shifted from 1.0 ± 0.4 ml/100 g at baseline to 3.7 ± 1.4, 4.1 ± 1.1, and 4.2 ± 0.9 ml/100 g at 15, 30, and 60 min of reperfusion, respectively (all P < 0.05). The diastolic volume intercept was 8.2 ± 0.7 ml/100 g at baseline and remained unchanged during reperfusion. Therefore, the difference of the systolic-diastolic volume intercepts, an index of elastic recoil forces, was decreased to 57 ± 8, 49 ± 7, and 47 ± 9% of baseline values (P < 0.05). The shift of the systolic pressure-volume relationship was accompanied by a transient decrease of contractile efficiency (slope of O2 consumption-pressure-volume-area relationship) at 15 min of reperfusion (from 43 ± 6 to 27 ± 7%). We hypothesize that the rightward shift of the systolic pressure-volume relationship was compatible with a decrease of elastic-restoring forces, probably induced by alterations in the extracellular collagen matrix and/or the cytoskeleton, and thereby our data imply that left ventricular dysfunction of postischemic myocardium does not result solely from disturbances in excitation-contraction coupling. Reprinted by permission of the publisher.