Long-term inhibition of myocardial
infarction by postconditioning
during reperfusion |
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Authors: | J Mykytenko F Kerendi J G Reeves H Kin A J Zatta R Jiang R A Guyton J Vinten-Johansen Z-Q Zhao |
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Institution: | (1) Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center/ Crawford Long Hospital Emory University School of Medicine, 550 Peachtree Street NE, Atlanta (GA), 30308-2225, USA |
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Abstract: | Cardioprotection with postconditioning has been well demonstrated
after a short period of reperfusion. This study tested the hypothesis
that postconditioning reduces infarct size, vascular dysfunction, and neutrophil
accumulation after a long-term reperfusion. Canines undergoing 60
min left anterior descending artery (LAD) occlusion were divided into two
control groups of either 3 h or 24 h of full reperfusion and two postconditioning
groups with three 30 s cycles of reperfusion and re-occlusion applied
at the onset of either 3 h or 24 h of reperfusion. Size of the area at risk (AAR)
and collateral blood flow during ischemia were similar among groups. In
controls, infarct size as percentage of the AAR (30 ± 3 vs. 39 ± 2* %) by TTC
staining, superoxide anion generation from the post-ischemic coronary arteries
by lucigenin-enhanced chemiluminescence (89 ± 5 vs. 236 ± 27* relative
light units (RLU/mg)], and neutrophil (PMN) accumulation by immunohistochemical
staining in the AAR (52 ± 11 vs. 84 ± 14* cells/mm2
myocardium) significantly increased between 3 and 24 h of reperfusion.
Postconditioning reduced infarct size (15 ± 4† and 27 ± 3.6† %), superoxide
anion generation (24 ± 4† and 43 ± 11† RLU/mg), and PMN accumulation
(19 ± 6† and 45 ± 8† cells/mm2 myocardium) in the 3 and 24 h reperfusion
groups relative to time-matched controls. These data suggest that myocardial
injury increases with duration of reperfusion; reduction in infarct size
and attenuation in inflammatory responses with postconditioning persist after
a prolonged reperfusion. * p < 0.05 24 vs. 3 h control; † p < 0.05 postconditioning
vs. time-matched control. |
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Keywords: | infarct size postconditioning reperfusion injury endothelial dysfunction neutrophils |
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