The Lazarus Heart

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heart muscle and insinuate themselves into the tangle of dying and in-

jured cells. To a biologist this sight is bizarre, uncanny. It's as though

the engine of a passing car could walk up to a stranded truck, climb

under the hood, and drive it away.

Farther away from the wound surface, the red cells also spill out their

nuclei, but these cell yolks clump together, fusing their remaining

cytoplasm to form a syncytium. Still farther away from the center of

action, the red cells undergo the more leisurely dedifferentiation we ob-

served in our frog fractures and DC culture studies. They turn into

primitive ameboid cells that move toward the area of damage and attach

themselves by pseudopods to the injured muscle fibers. In all of biology

there's no precedent for these virtuosic cellular metamorphoses. In fact,

they're so strange that most researchers have simply refused to believe in

their existence or try the experiment for themselves.

All these changes are well under way within fifteen minutes. Soon

afterward the extruded nuclei, the interconnected syncytial nuclei, and

the ameboid cells are all dividing as fast as they can, building up the

blastema. It's fully formed within three hours after the injury. By then

its cells have already started to redifferentiate into new heart-muscle

cells, synthesizing their orderly arrays of contractile fibers and con-

necting up with the intact tissue. If the clot contained more blood cells

than were needed, the extras outside of the area now degenerate, appar-

ently so as not to get in the way of the the repair work.

Meanwhile, the newt has survived by absorbing dissolved oxygen from