Linked Life Data

1335885

Source:http://linkedlifedata.com/resource/pubmed/id/1335885

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1993-2-9
pubmed:abstractText
This study examines the possibility that polymorphonuclear leukocyte activation, which can cause endothelial injury, may contribute to the capillary closure of diabetic retinopathy. To examine diabetes-related alterations in polymorphonuclear leukocyte activation, we compared the production of superoxide radical by these cells from normal and from diabetic cats that were maintained hyperglycemic. Polymorphonuclear leukocytes isolated from five diabetic and five normal cats were stimulated with 10 ng ml-1 phorbol myristate acetate, and the maximum rate of their superoxide radical production was measured spectrophotometrically. Stimulated polymorphonuclear leukocytes from diabetic cats generated more superoxide radical, at significantly higher rates, than did those from normals (3.32 +/- 0.33 and 2.50 +/- 0.41 nmol O2- min-1 10(-6) cells, respectively; P < 0.02). While addition of insulin or glucagon did not alter stimulated polymorphonuclear leukocyte radical production, glucose in high concentration did mildly impair its production in both groups. The exaggerated respiratory burst of polymorphonuclear leukocytes in diabetes could contribute to microvascular injury in the retina as well as in other tissues.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0014-4835
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
767-73
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Enhanced superoxide radical production by stimulated polymorphonuclear leukocytes in a cat model of diabetes.
pubmed:affiliation
Department of Ophthalmology, Duke University, Durham, NC.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't