Reduced tolerance of global ischemia in the hypertrophied heart. Effect of coronary flow regulation during reperfusion on postischemic recovery.
OBJECTIVE
Reduced coronary reserve during reperfusion may cause postischemic diastolic dysfunction in pressure-overload-induced hypertrophy. We studied the effect of coronary flow regulation (simulated hyperemic or depressed flow) on postischemic cardiac function during reperfusion.


METHODS
Left ventricular pressure overload was induced in 4-week-old rats by abdominal aortic constriction. At 6 weeks of age, isolated Langendorff-perfused hearts (perfusion pressures: 75 mmHg in controls and 110 mmHg in the aortic constriction group) were subjected to hypothermic global ischemia (15 degrees C, 210 min), followed by 2 types of coronary flow regulation during the initial 20 min of reperfusion--manipulated high flow in control hearts (group I), manipulated low flow in control hearts (group II), manipulated high flow in aortic constriction hearts (group III), and manipulated low flow in aortic constriction hearts (group IV) (n = 6/group), and then constant pressure perfusion during the subsequent 45 min of reperfusion. Cardiac function was measured using an isovolumic balloon in the pre- and postischemic periods.


RESULTS
Aortic constriction hearts exhibited greater left ventricular end-diastolic pressure than did control hearts. The increase in left ventricular end-diastolic pressure did not differ between group I (3 +/- 2 mmHg) and group II (-1 +/- 1 mmHg) or between group III (29 +/- 5 mmHg) and group IV (30 +/- 6 mmHg). No difference was seen in postischemic recovery of left ventricular systolic pressure between high and low flow groups in control and aortic constriction hearts.


CONCLUSIONS
Manipulations in coronary flow during reperfusion did not affect postischemic cardiac function in control or aortic constriction hearts, suggesting that depressed coronary flow during early reperfusion is not a primary cause of postischemic diastolic dysfunction in the hypertrophied myocardium.
Yamamoto
H
H
First Department of Surgery, Asahikawa Medical University, Hokkaido, Japan.
Yamamoto
F
F
Goh
K
K
Sasajima
T
T
D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology*; D003326:Coronary Circulation; D006321:Heart / Q000503:physiopathology; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D051381:Rats; D017208:Rats, Wistar