Biomedical Engineering Reference
In-Depth Information
in mice. h e signii cant increase in the A
2A
R in rats exposed to 4 ATA suggests that
A
2A
R may dampen inl ammatory damage associated with decompression sickness.
It would be interesting to determine whether inducers of adenosine minimize the
ef ects of DCS as they have I/R injury.
Key Points
• Activation of A
2A
R at the onset of hypoxic tissue injury would lessen the
damaging ef ects of inl ammation.
• Signii cant increases in expression of A
2A
R, which modulates inl ammation
by downregulating production of these cytokines, were detected only in
the quadriceps removed at 24 hr at er decompression from 4 ATA (Bigley
et al.
2008).
Definitions
Adenosine is a nucleoside composed of a molecule of adenine attached to a ribose
sugar molecule. Adenosine plays an important role in energy transfer, in signal
transduction as cyclic adenosine monophosphate, as an inhibitory neurotransmitter.
Adenosine is also a cryoprotector in preventing tissue damage from hypoxia and
ischemia. Adenosine signals via four known receptors (A
1
, A
2A
, A
2B
, and A
3
),
but adenosine activation of the A2A receptor is classii ed as anti-inl ammatory,
suppressing production of inl ammatory cytokines (Sullivan 2003).
SUMMARY
• Tissue injury triggers tissue hypoxia and inl ammation, which, in turn,
initiate CAM changes in DCS and I/R injury.
• Expression of CAMs is upregulated on injured/inl amed vascular
endothelia.
• Blood leukocytes transmigrate into the injured tissue sites through
endothelia by attaching to endothelial co-receptor ligands for specii c
CAMs.
• Inducers of increased CAM expression by vascular endothelia include
noxious tissue injury products (reactive oxygen species) as well as molecules
secreted by the inl ammatory blood cells and inl amed endothelia cells
(inl ammatory cytokines).
• A model is proposed that integrates the role of CAMs in inl ammatory
injury and mononuclear cell transmigration through endothelium into
injured tissue sites.
