Linked Life Data

8439001

Source:http://linkedlifedata.com/resource/pubmed/id/8439001

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2A Suppl
pubmed:dateCreated
1993-3-23
pubmed:abstractText
Although hemorrhage is known to cause increased susceptibility to infection, the precise mechanism remains unknown. Regional hypoxia due to reduced blood flow following hemorrhage appears to be a primary mediator that initiates the cascade of events leading to immunodepression and increased susceptibility to infection. This was evident from depression of lymphocyte functions, production of various lymphokines, macrophage expression of receptors involved in opsonin-mediated phagocytosis, and antigen presentation function of peritoneal, splenic, and Kupffer cells following hemorrhage. The depression in various immune functions is apparent immediately after hemorrhage and persists for a prolonged period of time, despite volume resuscitation. Furthermore, it appears that the increased release of systemic mediators, such as interleukin-1 (IL-1), IL-6, tumor necrosis factor, transforming growth factor type beta, and prostaglandin E2 is associated with marked depression in immune responses and increased susceptibility to infection following hemorrhage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9610
pubmed:author
pubmed:issnType
Print
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59S-67S
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Mechanism of increased susceptibility to infection following hemorrhage.
pubmed:affiliation
Department of Surgery, Michigan State University, East Lansing 48824.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review