Myocardial energetics and cardiac function of preserved rat heart.
We studied mitochondrial function in relation to ATP production and its relationship with myocardial oxygen consumption (VO2) and total mechanical energy using isolated rat hearts after 8, 12, and 24 h of hypothermic preservation. In isovolumic contraction, ventricular contractility and total mechanical energy were respectively assessed by the end-systolic elastance (Ees) and pressure-volume area (PVA). Ees significantly decreased after hypothermic ischemia, although the difference was not significant between 8 and 12 h. In contrast, VO2 measured at each left ventricular volume increased after hypothermic ischemia. PVA and VO2 were found to stay in linear correlation after prolonged hypothermic ischemia, although VO2 at null PVA and VO2 to PVA ratios significantly increased after hypothermic ischemia, especially after 12-h ischemia. Mitochondrial oxidative phosphorylation significantly decreased after hypothermic ischemia for longer than 12 h. These results indicate that mitochondrial oxidative phosphorylation was impaired due to long time hypothermic ischemia especially after 12-h ischemia. We conclude that energy uncoupling between VO2 and PVA in hypothermically preserved heart is attributable to disturbed mitochondrial oxidative phosphorylation and that 8 h is a critical point for efficient conversion of energy from VO2 into PVA in rat heart.
Kuwabara
M
M
Second Department of Surgery, Miyazaki Medical College, Japan.
Maruyama
H
H
Onitsuka
T
T
Koga
Y
Y
D000818:Animals; D003080:Cold Temperature; D003327:Coronary Disease / Q000378:metabolism*; D004195:Disease Models, Animal; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D015424:Reperfusion; D013599:Systole