Myocardial Cell Death (Apoptosis)

Technique

Myocardial Cell Death or Apoptosisis a distinct type of cell death that differs from necrosis in nature and biologic significance Apoptosis: a basic biological phenomenon with wide ranging implications in tissue kinetics and is considered a highly regulated and active process that contributes to biologic homeostasis.

why it is used

This type of cell death is most often associated with cells that are progressing through the cell cycle; thus, it has generally been believed that under physiologic conditions, apoptosis does not occur in terminally differentiated normal adult cells such as myocytes. Recent studies have demonstrated that myocardial cell apoptosis can be induced by a variety of insults, including hypoxemia , acute ischemia-reperfusion , myocardial infarction , cardiomyopathic end-stage heart failure and myocardial pressure stretch Although apoptosis contributes to myocardial cell death in the ischemia-reperfused heart, the molecular basis of apoptosis is poorly understood.

Alternative Methods

Apoptosis-inducing factor (AIF) has been characterized as a caspase-independent death effector. Upon the induction of apoptosis, mitochondrial AIF is released to the cytoplasm and then enters the nucleus, in which it induces chromatin condensation and 50 kbp DNA fragmentation. In the present study, we examined the role of AIF in ischemia-reperfusion injury in isolated rat hearts. AIF was detected in the cytosolic and nuclear fractions of hearts subjected to ischemia-reperfusion, whereas it was detected only in the mitochondria of control hearts. Moreover, AIF release increased in a reperfusion time-dependent manner. Pulse field gel electrophoresis revealed that 50 kbp DNA fragments were produced by ischemia/reperfusion.

Underlying pathology

In contrast, cytochrome c release and the activation of caspase-3 did not occur to a significant extent. Moreover, ischemic preconditioning attenuated the AIF release and the 50 kbp DNA fragmentation. These results suggest that AIF-dependent apoptosis is likely to attribute to myocardial cell death in the ischemia-reperfused heart and that it is related with the protective effect of ischemic preconditioning. ( Searle, 242)

Measurements of Regional Myocardial Function

The renin-angiotensin system is upregulated with diabetes, and this may contribute to the development of a dilated myopathy. Angiotensin II (Ang II) locally may lead to oxidative damage, activating cardiac cell death. Moreover, diabetes and hypertension could synergistically impair myocardial structure and function. Therefore, apoptosis and necrosis were measured in ventricular myocardial biopsies obtained from diabetic and diabetic-hypertensive patients. Accumulation of a marker of oxidative stress, nitrotyrosine, and Ang II labeling were evaluated quantitatively. The diabetic heart showed cardiac hypertrophy, cavitary dilation, and depressed ...