Biomedical Engineering Reference
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into rat infarction models. At four weeks after transplantation, the
engineered myocardial tissue shows compact and well-differentiated
tissue-derived cardiac muscle, whose thickness is 443 ± 32 µm,
covering the infarcted myocardium. Well-organized sarcomeres and
blood vessels, including endothelial cells (ECs) and smooth muscle
cells, which must be of donor origin, are observed in the implanted
grafts, and erythrocytes are also detected in the vessels, showing
that the vessels are connected to the host vasculature and the
connections must contribute to the long-term survival of implanted
tissue grafts. A point stimulation for transplanted myocardial tissues,
expect noncontractile myocardial tissue, which is observed in their
formaldehyde-fixed myocardial tissue or noncardiomyocyte grafts,
propagates as an electrical response to the remote myocardium,
showing the establishment of electrical coupling between the host
myocardium and the implanted graft. Because implanted grafts
can be uncoupled after acidification (pH 6.7) of the heart, the
electrical coupling between the implanted tissue graft and the host
myocardium is direct and normal but not in subnormal graft-host
coupling. In addition, telemetric electrocardiographic recordings
show that the transplantation of a myocardial tissue graft hardly
increases arrhythmias, and the circadian rhythms of recipient rats
are restored after transplantation. After infarction treatment, while
in the sham-operation control group, the increase of (1) LV end-
diastolic dimension (LVEDD), (2) LV end-diastolic pressure (LVEDP),
and (3) relaxation (tau) and (4) the decrease of fractional area
shortening (FAS) are observed, the engineered-tissue-grafted group
shows (1) maintenance of low-level values of LVEDD, LVEDP, and
tau and (2) improvement of FAS. In addition, the therapeutic effects
of engineered-myocardial-tissue transplantation are higher than
those of noncontractile-graft transplantation. These results show
that large-size pulsatile myocardial tissue shows electrical coupling
with the host myocardium without arrhythmia and survives for
a long time via functional anastomosis with the host vessels after
transplantation and contributes to myocardial regeneration and
cardiac function improvements, which is higher than expected
efficiency from paracrine effects.
Ott et al. have reconstructed 3D myocardial tissue by using
neonatal rat cardiac cells and a rat whole myocardium, which are
decellularized by coronary perfusion using a modified Langendorff
apparatus with detergents [23]. Sodium dodecyl sulfate (SDS)
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