DocumentCode
2094488
Title
An elementary analysis of physiologic shock and multi-organ failure: The Autodigestion Hypothesis
Author
Schmid-Schonbein, G.W. ; DeLano, F.A. ; Penn, A.H. ; Kistler, E.
Author_Institution
Dept. of Bioeng., Univ. of California San Diego, La Jolla, CA, USA
fYear
2012
fDate
Aug. 28 2012-Sept. 1 2012
Firstpage
3114
Lastpage
3115
Abstract
Physiological shock and subsequent multi-organ failure is one of the most important medical problems from a mortality point of view. No agreement exists for mechanisms that lead to the relative rapid cell and organ failure during this process and no effective treatment. We postulate that the digestive enzymes synthesized in the pancreas and transported in the lumen of the small intestine as requirement of normal food digestion play a central role in multi-organ failure. These powerful enzymes are usually compartmentalized in the lumen of the intestine by the mucosal barrier, but may escape into the wall of the intestine if the permeability of the mucosal lining increases. Entry of the digestive enzymes into the wall of the intestine precipitates an autodigestion process as well as an escape of pancreatic enzymes and breakdown products generated by them into the system circulation. The consequence of autodigestion is multiorgan failure. We discuss the possibility to block the digestive enzymes in acute forms of shock as a potential therapeutic intervention.
Keywords
biological organs; cellular transport; enzymes; permeability; autodigestion hypothesis; digestive enzymes; lumen; medical problem; mortality; mucosal barrier; multiorgan failure; pancreas; permeability; physiologic shock; small intestine; Biochemistry; Educational institutions; Electric breakdown; Electric shock; Electronic mail; Intestines; Humans; Intestines; Multiple Organ Failure; Pancreas; Shock;
fLanguage
English
Publisher
ieee
Conference_Titel
Engineering in Medicine and Biology Society (EMBC), 2012 Annual International Conference of the IEEE
Conference_Location
San Diego, CA
ISSN
1557-170X
Print_ISBN
978-1-4244-4119-8
Electronic_ISBN
1557-170X
Type
conf
DOI
10.1109/EMBC.2012.6346623
Filename
6346623
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