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the water through its skin. Now, at about the four-hour mark, there are
enough new muscle cells to withstand contraction, and the heart begins
pumping again, slowly. After five or six hours, most of the blastema cells
have redifferentiated into muscle, which is still somewhat "lacy" or deli-
cate compared with the established tissue. After about eight or ten hours,
however, the heart is virtually normal in appearance and structure, and
after a day it's indistinguishable from an uninjured one.
Why did we see this colossal regeneration, while the Oberprillers
found only a tiny, slow healing response in the salamander heart? Appar-
ently this was another manifestation of the Polezhaev principle. We
made a big wound; they made a small one. Only massive damage un-
leashed the full power of the cells.
Is this fantastic cellular power forever restricted to salamanders, or
does it reside latent in us, ready at the appropriate impetus to repair
damaged hearts without problem-filled (and frightfully expensive) trans-
plants of donated or artificial pumps? We don't know, but we've found
no other regenerative process that's forever off limits to mammals. At
this point we can only speculate on how such a treatment might be
accomplished, but at least the idea isn't wholly fantasy.
The first job is to identify human target cells able to dedifferentiate
into primitive totipotent cells. Bone marrow cells or immature eryth-
rocytes, the nearest equivalents to amphibian nucleated red blood cells,
are one obvious candidate population, especially since they seem to be
the crucial cells in rat limb regeneration and the inner part of fracture
healing. Fibroblasts despecialized by electrically injected silver ions
might be used. Another possibility is lymphocytes, one class of infec-
tion-fighting white blood cells. In our lab we've demonstrated that they,
too, can dedifferentiate in response to appropriate electrical stimuli.
Since newt-type heart regeneration doesn't occur naturally in mam-
mals, we would probably have to grow a large mass of the target cells in
tissue culture. Then, with the patient on a heart-lung machine, the
surgeon could cut away scar tissue and otherwise freshen the wound if it
wasn't recent enough, then apply enough of these ready-made pre-
blastema cells to fill the defect. They would be held in place by a blood
clot, sutured pericardium, or some type of patch. Then, assuming we'd
learned the electrical parameters already, electrodes would induce nu-
clear extrusion, dedifferentiarion, consolidation with surrounding mus-
cle, and the final transformation into normal cardiac muscle. The current
would probably have to be adjusted throughout the process to get
us
various
steps
in synchrony, and vitamins or drugs might be used to
enhance mitosis or protein synthesis. Once the scar had been removed,