Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
314
pubmed:dateCreated
1995-9-14
pubmed:abstractText
Although the success rate of microvascular replantation and revascularization procedures has increased steadily since the 1960s, some replanted tissues do not reperfuse despite technically adequate arterial anastomoses. This failure of microvascular perfusion is termed no reflow. Much research has been directed toward discovering the etiology of no reflow since it was first described 25 years ago. Three pathophysiologic processes have been identified as playing a central role in the development of no reflow: intracellular calcium overload, oxygen-free radical medicated damage, and altered arachidonic acid metabolism. The first tissue believed to be injured irreversibly by these processes is the endothelium, which leads to dysfunction of the parenchymal cells. All 3 pathways are interrelated extensively, which allows for pharmacologic intervention at many different steps. Agents that have been shown to be beneficial in preventing no reflow include calcium channel blockers, prostaglandin analogs, thromboxane synthesis inhibitors, vasodilators, thrombolytics, and many antioxidants. Although they have been shown to be effective in various laboratory models, additional investigation is necessary before these treatments can be established in clinical use.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0009-921X
pubmed:author
pubmed:issnType
Print
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
122-33
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Pathophysiology and related studies of the no reflow phenomenon in skeletal muscle.
pubmed:affiliation
Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
pubmed:publicationType
Journal Article, Review