monadnock
05-09-07, 09:35 AM
May 7, 2007 issue - Consider someone who has just died of a heart attack. His organs are intact, he hasn't lost blood. All that's happened is his heart has stopped beating—the definition of "clinical death"—and his brain has shut down to conserve oxygen. But what has actually died?
As recently as 1993, when Dr. Sherwin Nuland wrote the best seller "How We Die," the conventional answer was that it was his cells that had died. The patient couldn't be revived because the tissues of his brain and heart had suffered irreversible damage from lack of oxygen. This process was understood to begin after just four or five minutes. If the patient doesn't receive cardiopulmonary resuscitation within that time, and if his heart can't be restarted soon thereafter, he is unlikely to recover. That dogma went unquestioned until researchers actually looked at oxygen-starved heart cells under a microscope. What they saw amazed them, according to Dr. Lance Becker, an authority on emergency medicine at the University of Pennsylvania. "After one hour," he says, "we couldn't see evidence the cells had died. We thought we'd done something wrong." In fact, cells cut off from their blood supply died only hours later.
But if the cells are still alive, why can't doctors revive someone who has been dead for an hour? Because once the cells have been without oxygen for more than five minutes, they die when their oxygen supply is resumed. It was that "astounding" discovery, Becker says, that led him to his post as the director of Penn's Center for Resuscitation Science, a newly created research institute operating on one of medicine's newest frontiers: treating the dead.
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
As recently as 1993, when Dr. Sherwin Nuland wrote the best seller "How We Die," the conventional answer was that it was his cells that had died. The patient couldn't be revived because the tissues of his brain and heart had suffered irreversible damage from lack of oxygen. This process was understood to begin after just four or five minutes. If the patient doesn't receive cardiopulmonary resuscitation within that time, and if his heart can't be restarted soon thereafter, he is unlikely to recover. That dogma went unquestioned until researchers actually looked at oxygen-starved heart cells under a microscope. What they saw amazed them, according to Dr. Lance Becker, an authority on emergency medicine at the University of Pennsylvania. "After one hour," he says, "we couldn't see evidence the cells had died. We thought we'd done something wrong." In fact, cells cut off from their blood supply died only hours later.
But if the cells are still alive, why can't doctors revive someone who has been dead for an hour? Because once the cells have been without oxygen for more than five minutes, they die when their oxygen supply is resumed. It was that "astounding" discovery, Becker says, that led him to his post as the director of Penn's Center for Resuscitation Science, a newly created research institute operating on one of medicine's newest frontiers: treating the dead.
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