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Articles in PresS, published online ahead of print October 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00132.2002
Submitted on February 21, 2002
Accepted on September 23, 2002
1 Department of Medicine and The Emergency Resuscitation Center, The University of Chicago, Chicago, IL, USA
* To whom correspondence should be addressed. E-mail: khamann{at}medicine.bsd.uchicago.edu.
While ischemia/reperfusion (I/R) can initiate apoptosis, the timing and contribution of the mitochondrial/cytochrome c apoptosis death pathway to I/R injury is unclear. We studied the timing of cytochrome c release during I/R and whether subsequent caspase activation contributes to reperfusion injury in confluent chick cardiomyocytes. One hr simulated ischemia followed by 3 hr reperfusion resulted in significant cell death, with most cell death evident during the reperfusion phase, and demonstrating mitochondrial cytochrome c release within 5 min after reperfusion. By contrast, cells exposed to prolonged ischemia for 4 hr had only marginally increased cell death and no detectable cytochrome c release into the cytosol. Caspase activation could not be detected after ischemia only, but it significantly increased after reperfusion. Caspase inhibitors (zVAD-fmk, Ac-DQTD-CHO, or zLEHD-fmk) given only at reperfusion significantly attenuated cell death and resulted in return of contraction. Antixoxidants decreased cytochrome c release, nuclear condensation and cell death. These results suggest that reperfusion oxidants initiate cytochrome c release within minutes, and apoptosis within hours significant enough to increase cell death and contractile dysfunction.
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