title: Enhanced coronary vascular turgor effect on post-ischemic diastolic function in hypertrophied hearts.
abstract: 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.
authors: Department of Cardiovascular Surgery, Akita University School of Medicine, Hondo 1-1-1, Akita, 010-8543 Japan. h-yama@cvs.med.akita-u.ac.jp
authors: Hiroshi
authors: H
authors: Yamamoto
authors: Fumio
authors: F
authors: Yamamoto
authors: Hajime
authors: H
authors: Ichikawa
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003326:Coronary Circulation; D003971:Diastole; D004548:Elasticity; D006324:Heart Arrest, Induced; D006973:Hypertension / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D017725:Ventricular Pressure