Abstract：
:Vascular permeability and endothelial cell damage has been shown to occur in rats subjected to trauma with hemorrhagic-shock. Although the factors responsible for the endothelial cell injury are unknown, it has been hypothesized that toxic factors produced in response to hemorrhagic-shock originate in the gut and are absorbed into the mesenteric lymphatics. Consistent with this hypothesis, it has been shown that lymph collected from animals subjected to trauma with hemorrhagic-shock (T/HS) results in a marked decrease in endothelial cell viability both in vitro and in vivo. We therefore compared the lymph collected pre-T/HS to samples collected during, and up to 3h post-T/HS in order to identify a factor present or increased in post-T/HS lymph. This analysis revealed that a single cationic peptide band was significantly increased in post-T/HS lymph, but not in lymph from control animals subjected to trauma without hemorrhagic-shock (T/SS). This peptide was subsequently identified as the N-terminal 24 amino acids of rat serum albumin (RSA) by mass spectrometry and amino acid sequencing. Although the measured increase in the albumin peptide correlates with detectable shock lymph-induced endothelial cell toxicity, the peptide was not toxic to endothelial cells. We therefore propose that the significant increase in the albumin peptide is a marker for post-T/HS lymph-induced endothelial cell toxicity.
journal_name
Peptidesjournal_title
Peptidesauthors
Kaiser VL,Sifri ZC,Senthil M,Dikdan GS,Lu Q,Xu DZ,Deitch EAdoi
10.1016/j.peptides.2005.05.001subject
Has Abstractpub_date
2005-12-01 00:00:00pages
2491-9issue
12eissn
0196-9781issn
1873-5169pii
S0196-9781(05)00195-6journal_volume
26pub_type
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