Abstract
Langendorff perfused hearts were subjected to 15min of global no-flow ischemia and 30min reperfusion. Hearts of ovariectomised mice were hypercontractile at baseline compared with INT (+dP/dt, WT 6037± 416 vs. 5089± 537, TG 5526± 392 vs. 4975± 509mmHg/ms; P< 0.05). This hypercontractility in OVX hearts was maintained postischemia, and for WT hearts this was associated with a reduced efficiency of contractile function (0.53± 0.14 vs. 0.11± 0.01 nmolO2/(mmgHg)) and a greater incidence (50% vs. 6% of hearts) and duration (29.9± 13.3 vs. 26.7± 0.2 s; P< 0.05) of mechanical alternans, relative to INT. TG hearts exhibited greater functional recovery and fewer arrhythmia compared to WT. FO did not enhance recovery after ischemia in all groups. These data suggest that the intrinsic adaptive properties of the local cardiac endocrine environment modulate the impact of ovarian hormone withdrawal on myocardial function and metabolism. The unexpected finding that FO did not appear to enhance post-ischemic recovery in female hearts suggests that the nature of the molecular/functional adaptations underpinning altered cardiac excitation–contraction coupling in FO feedingmay be sexspecific. doi:10.1016/j.hlc.2008.05.572
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