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knockout and wild-type mice
1 Department of Veterinary Biosciences, University of Illinois, Urbana-Champaign, Illinois 61802, and 2 Departments of Biochemistry and Child Health, University of Missouri, Columbia, Missouri 65211
We
investigated the function of estrogen receptor-
in global myocardial
ischemia and reperfusion injury in male estrogen receptor-
knockout (ERKO) and wild-type mice. Mouse hearts were subjected to 45 min of global ischemia followed by 180 min of reperfusion. The
hearts were excised, cannulated, and maintained in a chilled (4°C)
cardioplegia solution until warm (37°C) oxygenated Krebs-Henseleit
bicarbonate buffer was perfused through the coronary arteries. ERKO
hearts started beating later and had a higher incidence of ventricular
fibrillation and/or tachycardia than control hearts. Coronary flow rate
was significantly lower in ERKO hearts during the 90- and 120-min
periods of reperfusion. Ca2+ accumulation was significantly
greater following 30, 90, 120, 150, and 180 min of reperfusion in ERKO
hearts. Nitrite production was significantly less in ERKO hearts
following 90, 120, and 150 min of reperfusion. Myocardial reduction of
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was
significantly lower in experimental ERKO hearts. Marked interstitial
edema and contraction bands were seen in hematoxylin-eosin-stained sections of ischemia-reperfused ERKO hearts but not in control tissues. Hematoxylin-basic fuchsin-picric acid-stained sections from
experimental ERKO hearts had fewer viable myocytes compared with
controls. Transmission electron microscopy revealed swollen and
fragmented mitochondria with amorphous and granular bodies, loss of
matrix, and rupture of cristae in experimental ERKO hearts. This is the
first demonstration that estrogen receptor- plays a cardioprotective
role in ischemia-reperfusion injury in males.
calcium; nitric oxide; mitochondrial function; myocardial ultrastructure
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