title: Separation of inherent diastolic myocardial fiber tension and coronary vascular erectile contributions to wall stiffness of rabbit hearts damaged by ischemia, hypoxia, calcium paradox and reperfusion.
abstract: Ischemic myocardial contracture is exacerbated by reperfusion. This study examines the extent to which intensification of contracture by reperfusion is due to metabolic reoxygenation phenomena or hydraulic erectile contributions of coronary perfusion to left ventricular (LV) stiffness. Isolated rabbit hearts, with fluid-filled LV intraventricular baloons, were subjected either to: control aerobic perfusion; 30 or 60 min of global ischemia; 60 min of hypoxia with constant coronary flow; or 10 min of calcium-free perfusion to cause calcium paradox injury. During reperfusion with control perfusate isovolumic LV end diastolic pressure (LVEDP) was measured with constant coronary flow and during transient, 1 min, total global ischemia to measure the contribution of the coronary perfusion to LVEDP. In all injured groups LVEDP was increased compared to control hearts. The decrease in LVEDP during transient ischemia was greater in damaged hearts than in controls, demonstrating a greater contribution of coronary perfusion to LVEDP after injury. Only in the hypoxic hearts did diastolic fiber tension increase upon reperfusion. Inherent diastolic fiber tension decreased during 15 to 60 min of reperfusion in the ischemic and hypoxic injury groups, a trend which was masked by an increasing effect of coronary perfusion on LV chamber stiffness. During the reperfusion period enhancement of the erectile effect was more pronounced at higher preloads. Thus, reperfusion contracture was maintained both by changes in inherent fiber stiffness and by changes in the erectile effect. These contributions changed over time and varied with the type and severity of injury, but after all types of injury the erectile vascular effect made a greater contribution to diastolic chamber stiffness than inherent fiber tension.
authors.forename: W M
authors.initials: WM
authors.lastname: Vogel
authors.forename: L L
authors.initials: LL
authors.lastname: Briggs
authors.forename: C S
authors.initials: CS
authors.lastname: Apstein
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000502:physiology*; D003187:Compliance; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D003971:Diastole; D004548:Elasticity; D006352:Heart Ventricles / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D007473:Ion Channels / Q000502:physiology; D009200:Myocardial Contraction; D010477:Perfusion; D011817:Rabbits; D013599:Systole
chemical_list: D007473:Ion Channels; D002118:Calcium