while reading through many documents, I have seen an interesting subject..
apoptosis: meaning cell suicide wave that many cells start to kill themselves..
by mitochondria..
how this happen ? after a heart attack when cells are left without oxygene.. its an aftermath starting the whole atomic chain reaction by giving oxygene to the patient.. and interestingly not only heart is effected .. all organs..
"The mitochondrion, powerhouse of the cell, is the central player in defining the outcome of heart attacks. Mitochondria contain cellular poisons that are normally sequestered in inactive form, but when unleashed and activated they enforce cell suicide. These suicide regulators are released from mitochondria through
mitochondrial death channels. Understanding how the death channels work may hold the key to new treatments that could dramatically reduce myocardial injury and improve the outcome for patients who experience acute myocardial infarction.
A heart attack can affect 50 percent or more of the myocardial left ventricle (which takes in freshly oxygenated blood), causing massive tissue loss and scarring, which is known as infarction. Heart attacks begin with thrombosis; a blood clot wedged in a coronary artery causes reduced blood flow to downstream tissue (ischemia). The cardiac muscle becomes hypoxic (short of oxygen) and acidotic, and the energy level falls because the lack of oxygen interrupts mitochondrial metabolism. Cadiac tissue severely affected by ischemia may cease to contract. Ischemia must be relieved in a timely manner or all of the tissue downstream of the blood clot will die. Relief occurs when the flow of oxygenated blood to the tissue recommences, a process known as reperfusion. The amount of tissue salvaged by reperfusion is determined by the amount of time between the onset of ischemia and removal of the clot.
When reperfusion delivers oxygen back to the tissue, mitochondria become reenergized and contractions resume. If the ischemic period is short, damage to the heart may be minimal at the onset of reperfusion. However, lethal injury spreads insidiously across the formerly ischemic region over the hours, days and sometimes weeks after reperfusion. This damage, known as
reperfusion injury, was first described about 20 years ago. For many heart attack victims, it is the greatest threat to survival.
As reperfusion injury develops, heart cells are forced into a wave of suicide known as
apoptosis, or programmed cell death. The stimuli for this are a combination of the reoxygenation component of reperfusion and an imbalance of calcium ions and protons that develops during ischemia and which is exacerbated by reperfusion. The targets for both of these stimuli are the mitochondria. Reperfusion injury begins when mitochondrial death channels open and release the suicide activators. We are only now beginning to fully understand what causes the death channels to open and how the suicide process works.."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3163465/ 
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Topic: apoptosis (Read 6276 times)