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INJURY
TUGAS PRESENTASI PRABEDAH
OLEH:
1. AMALIA F ASHARI,
2. LUH PUTU NEOLITA PRADNYA W,
3. MENIK SAYEKTI,
VASCULAR ENDOTHELIUM
NEUTROPHIL-ENDOTHELIUM INTERACTION
• The inflammatory response to infection facilitates
neutrophil and other immunocyte increased
vascular permeability, chemoattractants & endothelial
adhesion factor as selectin
CHEMOKINES
GTP
Increased NO is also detectable in septic shock associated with low
peripheral vascular resistence and hypotension.
Increased NO in sepsis NOS activity and expression, cytokines
release inhibition of NO production seemed initially to be
severe sepsis
Prostacyclin
Prostacyclin (prostaglandin/PGI) is
derivered from arachidonic acid (AA),
nitric oxide (NO) is derived from L-
arginine. The increase cyclic
adenosine monophosphate(cAMP)
and cyclic guanosine
monophosphate(cGMP) results
smooth muscle relaxation and inhibit
platelets thrombus formation
ENDOTHELINS
Endothelins are potent mediators of vasoconstriction.
Endothelins composed of three members : ET-1, ET-2, ET-3. ET-1 synthesized
primarily by endothelial cells, is the most potent endogenous vasoconstrictor
Endothelins release is upregulated in response to hypotension, injury, anoxia
The natriuretic pptides, atrial natriuretic factor (ANF) & brain natriuretic peptides
(BNP) are family of peptides that are released primarily by atrial tissue
ANF and BNP increased in the setting of cardiac disorders, recent evidence
indicates some distinctions in the setting of inflammation
Elevated pro BNP has been detected in septic patient
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