The heart possesses the remarkable ability to adapt itself against any stressful situation by increasing resistance to the adverse consequences. Creating a stress reaction by repeated ischemia and reperfusion or subjecting the hearts to heat or oxidative stress enables the heart to meet the future stress challenge by upregulating its cellular defense through the direct accumulation of intracellular mediators that constitute the material basis of increased adaptation to stress. Thus, the powerful cardioprotective effect of adaptation is likely to originate at cellular and molecular levels (Das, 1996).
Ischemic preconditioning is the manifestation of the earlier stress response that occurs during repeated episodes of brief ischemia and reperfusion and can render the myocardium more tolerant to a subsequent potential lethal ischemic injury. This transient adaptive response has been demon-
Figure 4 Effects of ischemia and reperfusion on DNA fragmentation. DNA was isolated from hearts and subjected to 1.8% agarose gel electrophoresis. A 100-bp DNA ladder was used as a molecular weight marker (lane A). Lane B, baseline; C, 15 min ischemia; D, 15 min ischemia followed by 30 min reperfusion; E, 15 min ischemia followed by 60 min reperfusion; F, 15 min ischemia followed by 90 min reperfusion; and G, 15 min ischemia followed by 120 min reperfusion. Data reproduced with permission from Maulik et al. (1998e).
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