Wall tension and myocardial dysfunction after ischemia and reperfusion.
Cell viability is maintained during prolonged ischemia (ISCH) in isolated heart systems because mechanical function is nil (acute hibernation). By contrast, a noncontracting ischemic segment in an in vivo heart exhibits irreversible damage after < or = 30 min. To explore this difference, isolated rabbit hearts were buffer perfused and exposed to elevations of ventricular balloon pressure (BP) during ISCH to mimic systolic stresses of a dyskinetic (DYSK) segment. Relationships of magnitude and duration of stress to recovery of systolic function and metabolism were assessed. After 30 min of reperfusion (R30) in hearts subjected to 90 min of ISCH [10% coronary flow (CF)] and BP = 0, peak systolic pressure (PSP) returned to 69% of control. With BP set at 120 mmHg, recovery was to only 24%. With BP = 80, PSP at R30 was 46%. Extent of recovery was inversely affected by the duration of elevated pressure. Tissue ATP was reduced from 18.5 to 3.7 and glycogen from 164 to 28 mumol/g in the BP = 120 group. CF and myocardial O2 consumption were reduced to 50% at R30; there was a threefold increase in wall stiffness. These data suggest that mechanical stress of DYSK contributes significantly to metabolic and functional deterioration of ischemic myocardium.
Downing
S E
SE
Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510.
D000818:Animals; D001794:Blood Pressure; D003187:Compliance; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D011817:Rabbits; D013314:Stress, Mechanical; D013599:Systole; D016276:Ventricular Function