Biomedical Engineering Reference
In-Depth Information
tial platelet precipitation. The platelet-protein complex is eventually formed
via the intermediation of the Willebrand factor, a glycoprotein located on the
platelet cell membrane. Subsequently, the precipitated platelets experience
conformational change and secrete a series of bioactive substances (hor-
mones) including serotonin, cortin, ADP, and thromboxane A
2
[TXA
2
],which
further activates more platelets and catalyzes the production of thrombin,
finally resulting in platelet aggregation and thrombogenesis.
Neutrophil and Monocyte Infiltration
Implantation-related acute inflammatory reactions are usually caused by neu-
trophil adsorption onto the surfaces of synthetic implants, which is mostly
intermediated by the strong promoters of C
5
aandLeukotriencB
4
etc. Mono-
cytes in blood circulation are also prone to adsorb to the sites of blood vessel
defects or endothelium regeneration. With the stimulation by miscellaneous
activating factors in serum, monocytes tend to differentiate into macrophages
[M
] and become one of the major participators for host chronic inflamma-
tion.
φ
Limited Endothelial Cell Ingrowth and Smooth Muscle Cell Invasion
The continuous and orderly EC patterning generates the perfect integrity of
blood vessel endothelium and simultaneously functions to secrete bioactive
matter resisting thrombosis, initiating thrombolysis, and preventing SMC in-
vasion, thereby maintaining the normal rheology of blood flow. However,
from the border of synthetic implants suturing with native tissues, the EC
ingrowth is usually very limited. The maximal ingrowing depth is no more
than 1
2 cm and the area around incision anastomosis is frequently cov-
ered by injured and/or non-fused EC with abnormally varied biochemical
characteristics. Consequently, the uncovered portions of the material surface
severely induce in situ blood clotting and the SMC underneath the endothe-
lium is stimulated to overgrow leading to thrombogenic SMC invasion and
endothelium hyperplasia [84-87].
∼
1.3.2
Anti-Thrombogenic Coating
By summarizing the potential host reactions occurring at the blood-material
interface, the employment of improperly treated artificial implants will re-
sult in serious damage and even death of the host. An alternative method
relies on applying anti-coagulating/thrombolytic drugs, like heparin, to act
against thrombogenesis. However, this inevitably carries the risk of induc-
ing fatal bleeding and even the risk of a host systematic immuno-disorder.
Therefore, the fundamental solution still depends on the improvement of ma-
terials by surface modification. As discussed in Sect. 1.2.3, considering the
dilemma of material biocompatibility and mechanical strength, also balanc-
