Linked Life Data

16179531

Source:http://linkedlifedata.com/resource/pubmed/id/16179531

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2005-9-23
pubmed:abstractText
The central nervous system depends critically on a regular supply of oxygen and glucose for the formation of adenosine triphosphate (ATP) and the sustenance of its energy metabolism. Consequently, a significant reduction in the supply of oxygen and glucose to neuronal tissue causes an imbalance between the energy supply and demand, inducing the onset of neuronal ischemia and triggering many metabolic cascades leading to irreversible injury and cell death. Nicotinamide (NAm), an essential precursor to nicotinamide adenine dinucleotide (NAD+), which raises brain ATP levels, may improve cerebral blood flow and is neuroprotective against ischemia-induced injury. We therefore chose to examine the metabolic and electrophysiologic/functional effects of NAm (0.1 mM, 1.0 mM, 10.0 mM) under normal, control, and ischemic conditions, as well as following the early stages of reperfusion ("return-to-control" conditions) using an in vitro rabbit retina model where blood flow effects are excluded. Under nonischemic, control conditions, the protective concentration of NAm (10.0 mM) increased glucose utilization (34%, P < 0.01) and decreased lactate production (44%, P < 0.01), but had no significant effect on electrophysiologic function. After 2 h of ischemia, glucose utilization was significantly decreased (41%, P < 0.01) and lactate production was unaffected by NAm (10 mM). Following 3 h of "reperfusion", NAm (10 mM) significantly improved glucose utilization (217%, P < 0.01), lactate production (40%, P < 0.01), and electrophysiologic function (264%, P < 0.01) relative to controls. Thus, the functional neuroprotective effects of NAm may be independent of blood flow effects, but related, at least in part, to its improvement of tissue glucose utilization and lactate production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0077-8923
pubmed:author
pubmed:issnType
Print
pubmed:volume
1053
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
258-68
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Nicotinamide modulates energy utilization and improves functional recovery from ischemia in the in vitro rabbit retina.
pubmed:affiliation
Department of Ophthalmology, Beckman Vision Center, University of California, San Francisco, USA.
pubmed:publicationType
Journal Article, In Vitro