Publication: Effects of ischaemia-reperfusion and cyclosporin-A on cardiac muscle ultrastructure
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Date
1998
Authors
Jurado, F. ; Bellón, J.M. ; Pareja, J.A. ; Golittsin, A. ; Millán, L. ; Pascual, G. ; Buján, J.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The present study investigates the effects on
the cardiac muscle cell of two of the determining factors
for the success of organ transplant; ischaemia-perfusion
and immunosuppressive treatment with cyclosporin-A
(CsA). To this end an abdominal, heterotopic heart
transplant model in singenic Sprague-Dawley rats was
employed.
Three study groups were established: Group I
(control, n=15) animals undergoing heart transplant
without treatment; Group I1 (n=15) animals undergoing
heart transplant and subjected to a daily dose of CsA in a
cremophor vehicle (sandimunB) (5 mg/kg/sc); Group I11
(n=15): animals undergoing heart transplant and
administered a daily dose of pure CsA (5 mg/kg/sc).
Recipient animals were sacrificed 7, 14, 21, 30 and 50
days after transplant. During the post-operative period,
heart function was assessed by daily abdominal
palpation. Graft specimens obtained at each follow-up
period were subjected to light and transmission
electron microscopy. Immunohistochemical analysis of
specimens was performed using the rat macrophagespecific
monoclonal antibody MCA-341.
The ischaemia/reperfusion process induced
considerable alteration to cardiac muscle cells of control
animals. Effects, apparent after the first week of
transplant, included mitochondrial swelling and loss of
cristae, hypertrophy of the sarcoplasmic reticulum and
structural changes to sarcomeres. Two weeks after transplant, the myocardium was infiltrated by
inflammatory cells. These effects diminished 30 days
post-transplant. Cardiac tissues of treated animals
(groups I1 and 111) showed similar behaviour although, in
the latter group, mitochondrial damage was greater and
intense myocardial fibrosis took place. Infiltration of
cardiac muscle by white blood cells did not take place
until 3 weeks post-implant.
These results indicate: a) The ultrastructural changes
detected in cardiac fibres of animals of the three study
groups were attributable to the ischaemialreperfusion process rather than to treatment with CsA; b) CsA
appears to augment mitochondrial damage and
myocardial fibrosis; c) the inflammatory response was
delayed and reduced by the immunosupressant; and d)
the cremophor administration vehicle did not seem to
exert an independent toxic effect on the myocardium.
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