title: Loss of elastic recoil in postischemic myocardium induces rightward shift of the systolic pressure-volume relationship.
abstract: 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.
authors.affiliation: Experimental Cardiology, Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
authors.forename: R
authors.initials: R
authors.lastname: Krams
authors.forename: M
authors.initials: M
authors.lastname: Janssen
authors.forename: C
authors.initials: C
authors.lastname: Van der Lee
authors.forename: J
authors.initials: J
authors.lastname: Van Meegen
authors.forename: J W
authors.initials: JW
authors.lastname: De Jong
authors.forename: C J
authors.initials: CJ
authors.lastname: Slager
authors.forename: P D
authors.initials: PD
authors.lastname: Verdouw
mesh_terms: D000818:Animals; D003971:Diastole; D004548:Elasticity; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D066298:In Vitro Techniques; D007773:Lactates / Q000097:blood; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D011687:Purines / Q000097:blood; D013552:Swine; D013599:Systole; D013997:Time Factors
chemical_list: D007773:Lactates; D011687:Purines; D010100:Oxygen