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1 Experimental Research Laboratory, Division of Cardiology, University of Louisville and Jewish Hospital Heart and Lung Institute, Louisville, Kentucky 40292; and 2 Department of Biomedical Sciences, College of Allied Health, University of South Alabama, Mobile, Alabama 36688
Conscious rabbits underwent six
4-min occlusion and 4-min reperfusion cycles for 3 consecutive days
(day 1, 2, and 3); on day
1, rabbits received intravenous vehicle [preconditioning (PC)] (group I, n = 6), superoxide dismutase (SOD;
group II, n = 5), catalase (group
III, n = 6), or the hydroxyl radical (· OH)
and peroxynitrite (ONOO
) scavenger
N-2-mercaptopropionyl glycine (MPG [group IV],
n = 6). In the PC group, the recovery of systolic wall
thickening (WTh) after the sixth reperfusion was markedly improved on
days 2 and 3 compared with day 1 and
the total deficit of WTh was correspondingly reduced, indicating a late
PC effect against myocardial stunning. Neither SOD nor catalase had any
significant effect on the severity of stunning on day 1 or
on the development of late PC on days 2 and 3,
despite high plasma levels. In contrast, MPG markedly attenuated the
severity of stunning on day 1 and prevented the development
of late PC on day 2. Two additional groups of rabbits received an intracoronary infusion of vehicle (group V,
n = 4) or the reactive oxygen species (ROS) generating
solution [cumene hydroperoxide (CuOOH, group VI,
n = 7)] on day 0, and were then subjected
to the six occlusion/reperfusion cycles on days 1, 2, and
3. In group VI, infusion of CuOOH elicited a late
PC effect 24 h later (on day 1). Taken together, these
results demonstrate that oxidant species play an essential role in
triggering the development of late PC against stunning in conscious
rabbits. The fact that late PC was blocked by MPG and mimicked by CuOOH implicate ONOO and/or ·OH as the oxygen species
responsible for the initiation of this phenomenon. In addition, the
finding that exogenous ROS (CuOOH) reproduced the phenotype of late PC
indicates that ROS are not only necessary but also sufficient to
trigger this defensive adaptation of the heart to stress.
catalase; cumene hydroperoxide; myocardial ischemia-reperfusion; N-2-mercaptopropionyl glycine; reactive oxygen species; superoxide dismutase
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