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CARDIOVASCULAR
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Volume 3, 1998, No 2 |
Abstract:
The search for a noncalcifying tissue material having high
patentability to be used for valve replacement applications
continues to be a field of extensive investigation. The present
study describes the mineralization of glutaraldehyde-treated
bovine pericardium (GBP), in an extracirculatory environment and
the possible methods of prevention via certain antiplatelet
agents (like aspirin, vitamin C, B6,E and gentamycin). It seems
that the addition of these antiplatelet agents in the calcium
phosphate solutions, variably inhibited the GBP calcification.
Our earlier studies have shown that most of these drugs can
modulate fibrinogen surface attachment and subsequent platelet
adhesion. Further studies were performed on porcine pericardium
modified with polyethylene glycol and subsequently immobilizing
bioactive molecules like PGE1, hirudin or heparin via the
carbodiimide functionalities. Such novel interfaces demonstrated
dramatic reduction in fibrinogen adsorption, calcium deposition
and platelet attachment. It may be hypothesized that the influx
of calcium on GA treated pericardium may be due to the cellular
components or the involvements of plasma proteins like fibrinogen
molecule. The exact mechanisms are not well understood, however
more detailed studies are needed to understand the involvement of
plasma proteins and cellular components of the recipient blood in
tissue associated calcification.
Keywords:
pericardial calcification, antiplatelet agents, cellular
involvements, vitamins, gentamycin, PGE1, hirudin, heparin,
fibrinogen adsorption
Address for Correspondence:
Reference:
(CVE. 1998; 3 (2): 79-85)
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