We investigated the effects of estrogen on global myocardial ischemia-reper
fusion injury in rats that were ovariectomized (Ovx), sham-operated, or ova
riectomized and then given 17 beta -estradiol (E(2)beta) supplementation (O
vx+E(2)beta). Hearts were excised, cannulated, perfused with and then immer
sed in chilled (4 degreesC) cardioplegia solution for 30 min, and then retr
ogradely perfused with warm (37 degreesC), oxygenated Krebs-Henseleit bicar
bonate buffer for 120 min. The coronary flow rate, first derivative of left
ventricular pressure, and nitrite production were all significantly lower
in Ovx than in sham-operated or Ovx+E(2)b hearts. However, coronary flow ra
tes or nitrate production were not consistently different throughout the en
tire reperfusion period. Ca2+ accumulated more in Ovx rat hearts than in sh
am-operated or Ovx+E(2)beta hearts, and mitochondrial respiratory function
was lower in Ovx hearts than in hearts from the other two groups. Marked in
terstitial edema and contraction bands were seen in hematoxylin-eosin-stain
ed sections of Ovx rat hearts but not in hearts from either of the other gr
oups. Hematoxylin-basic fuchsin-picric acid-stained sections revealed fewer
viable myocytes in hearts from the Ovx group than from the sham or Ovx+E(2
)beta group. Transmission electron microscopy demonstrated more severely da
maged mitochondria and ultrastructural damage to myocytes in Ovx rat hearts
. Our results indicate that estrogen plays a cardioprotective role in globa
l myocardial ischemia-reperfusion injury in female rats.