OK, this is fascinating, big stuff. We’re on the verge of a huge breakthrough it sounds like:
Biologists are still grappling with the implications of this new view of cell death—not passive extinguishment, like a candle flickering out when you cover it with a glass, but an active biochemical event triggered by “reperfusion,” the resumption of oxygen supply. The research takes them deep into the machinery of the cell, to the tiny membrane-enclosed structures known as mitochondria where cellular fuel is oxidized to provide energy. Mitochondria control the process known as apoptosis, the programmed death of abnormal cells that is the body’s primary defense against cancer. “It looks to us,” says Becker, “as if the cellular surveillance mechanism cannot tell the difference between a cancer cell and a cell being reperfused with oxygen. Something throws the switch that makes the cell die.”
With this realization came another: that standard emergency-room procedure has it exactly backward. When someone collapses on the street of cardiac arrest, if he’s lucky he will receive immediate CPR, maintaining circulation until he can be revived in the hospital. But the rest will have gone 10 or 15 minutes or more without a heartbeat by the time they reach the emergency department. And then what happens? “We give them oxygen,” Becker says. “We jolt the heart with the paddles, we pump in epinephrine to force it to beat, so it’s taking up more oxygen.” Blood-starved heart muscle is suddenly flooded with oxygen, precisely the situation that leads to cell death. Instead, Becker says, we should aim to reduce oxygen uptake, slow metabolism and adjust the blood chemistry for gradual and safe reperfusion.