Enhanced coronary vascular turgor effect on post-ischemic diastolic function in hypertrophied hearts.

We investigated the effect of coronary perfusion pressure on post-ischemic left ventricular (LV) diastolic function in the hypertrophied heart. LV pressure overload was induced in four-week-old rats by abdominal aortic constriction (AC), with controls (C) undergoing sham operations. At six weeks of age, isolated Langendorff-perfused hearts (perfusion pressures: 75 and 110 mmHg in C and AC hearts, respectively) were subjected to hypothermic global ischemia (15 degrees C, 210 min) followed by 65 min of reperfusion (group I: C hearts subjected to aerobic perfusion alone, group II: C hearts subjected to ischemia/reperfusion, group III: AC hearts subjected to aerobic perfusion alone, group IV: AC hearts subjected to ischemia/reperfusion; n=6/group). LV end-diastolic pressure (LVEDP) at a constant balloon volume was assessed under perfusion pressures of 110, 75, and 0 mmHg during aerobic perfusion alone (groups I and III) or post-ischemic perfusion (groups II and IV). The LVEDP differences between perfusion pressures of 75 and 110 mmHg were 6.2+/-3.2, 3.2+/-2.7, 3.2+/-1.5, and 12.8+/-4.2* mmHg in groups I, II, III, and IV, respectively (*P<0.05 vs. group III). Pressure overload-induced hypertrophied hearts exhibit post-ischemic diastolic dysfunction, which may be caused partly by the enhanced coronary vascular turgor effect on myocardial stiffness.