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Protection from postconditioning has been documented in in situ
animal models and it has been proposed that it is targeting circulating leukocytes.
We therefore tested whether postconditioning can protect leukocytefree,
buffer–perfused rabbit hearts. Infarct size was measured with triphenyltetrazolium
staining. In control hearts undergoing 30 min of regional
ischemia and 2 h of reperfusion, 33.3 ± 2.2% of the risk zone infarcted. The
protocol previously used in open–chest animals of four postconditioning
cycles of 30 s reperfusion/30 s ischemia starting at the beginning of reperfusion
decreased infarction to only 24.8 ± 2.5% of the risk zone in these isolated
hearts. Because of the meager protection induced by four 30 s postconditioning
cycles, we evaluated the effect of postconditioning with 6 cycles of
10 s reperfusion/10 s ischemia starting at the beginning of reperfusion. Robust
salvage was seen with only 10.4 ± 3.4% of the risk zone infarcting (p < 0.001
vs control and p < 0.003 vs 4 cycles of 30 s ischemia). The 10s protocol was
used in all studies of signal transduction. Wortmannin (100 nM), a phosphatidylinositol
3– (PI3–) kinase antagonist, infused for 20 min starting 5 min
before reperfusion, blocked postconditionings, protection (31.2 ± 4.2%
infarction) as did 1H–[1,2,4]oxadiazole[4,3–a]quinoxalin–1–one (ODQ)
(2 µM) a guanylyl cyclase inhibitor (36.9 ± 5.3%) and 8–p–(sulfophenyl)
theophylline (SPT) (100 µM), a non–specific adenosine receptor blocker (34.2
± 2.8%). Thus, postconditionings protection is not dependent on circulating
blood factors or cells, and its anti–infarct effect appears to require PI3–kinase
activation, stimulation of guanylyl cyclase and occupancy of adenosine receptors.
These signaling steps have also been identified in preconditioning and
during pharmacologic cardioprotection and suggest commonality of a protective
mechanism.This revised version was published online in December 2004 with a minor correction to the article title 相似文献
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