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Cardiovascular and Pulmonary Research Institute, Allegheny University of the Health Sciences, Pittsburgh, Pennsylvania 15212
The goal of this study was to determine whether
the cardioprotective effects of an
A1-receptor agonist and ischemic
preconditioning (IPC) involve a shift in the pre-coronary artery
occlusion (CAO) spatial distribution of myocardial blood flow, which
might shed light on the mechanism of IPC and explain its heterogeneous
effects. Accordingly, 60 min of CAO followed by 72 h of coronary artery reperfusion (CAR) was examined in three groups of conscious pigs 10-14 days after instrumentation with aortic and left atrial
catheters and coronary artery occluders. Myocardial infarct size,
expressed as a fraction of the area at risk (AAR), was reduced
significantly (P < 0.05) by infusion
of the A1 agonist (27.1 ± 6.6%) and to a greater extent (P < 0.05) by IPC (11.6 ± 5.1%) compared with infarct size in
vehicle-treated animals (55.1 ± 2.9%). Transmural myocardial blood
flow (radioactive microspheres) in the AAR shifted toward lower levels
after infusion of the A1 agonist
(1.27 ± 0.19 vs. 0.74 ± 0.10 ml · min
1 · g
1)
or IPC (1.27 ± 0.11 vs. 0.96 ± 0.09 ml · min
1 · g
1)
but not after infusion of the vehicle (1.20 ± 0.10 vs. 1.23 ± 0.09 ml · min
1 · g
1).
This study demonstrated that both pretreatment with an adenosine A1 agonist and also IPC altered
the spatial distribution of pre-CAO myocardial blood flow, which might
reflect a downregulation of metabolic state and thus play a role in the
cardioprotective effects of IPC.
myocardial ischemia; infarction; coronary blood flow; myocardial stunning
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