Linked Life Data

12480820

Source:http://linkedlifedata.com/resource/pubmed/id/12480820

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2002-12-13
pubmed:abstractText
Dystrophin has a key role in striated muscle mechanotransduction. In mice lacking the gene encoding for dystrophin (mdx mice), the absence of dystrophin and several other proteins of the dystrophin-glycoprotein complex induces a defect in flow (shear stress)-mediated NO-dependent dilation (FMD). Because the endothelium is essential for the adaptation of arteries to chronic changes in blood flow, the long-term consequences of this vascular deficiency might affect flow-induced vascular remodeling. Thus, we submitted mouse mesenteric resistance arteries to chronic changes in flow by alternatively ligating arteries. Arteries were thus submitted to high flow (HF), low flow (LF), or normal flow. After 2 weeks, arteries were studied in vitro in an arteriograph. Increases in diameter (from 174+/-10 to 210+/-15 microm, pressure 75 mm Hg) found in HF arteries were not significant in mdx mice. Arterial diameters in LF arteries decreased similarly in control and mdx mice. FMD increased in HF arteries and decreased in LF arteries. FMD was not increased in HF arteries in mdx mice. NO-dependent FMD and NO synthase expression increased in the HF arteries of control mice but not in those of mdx mice. Dilatory and contractile tone, depending on the smooth muscle, was unaffected in HF arteries but decreased in LF arteries of both strains. We conclude that resistance arteries of mdx mice do not adapt properly to chronic changes in flow, inasmuch as the increases in diameter, endothelial NO synthase expression, and FMD did not occur in mdx mice submitted to HF for 2 weeks. This study suggests that blood flow regulation might be disturbed in dystrophin-related myopathies, possibly increasing organ damage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
13
pubmed:volume
91
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1183-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12480820-Adaptation, Physiological, pubmed-meshheading:12480820-Animals, pubmed-meshheading:12480820-Blood Flow Velocity, pubmed-meshheading:12480820-Blood Pressure, pubmed-meshheading:12480820-Disease Models, Animal, pubmed-meshheading:12480820-Dystrophin, pubmed-meshheading:12480820-Endothelium, Vascular, pubmed-meshheading:12480820-Ligation, pubmed-meshheading:12480820-Male, pubmed-meshheading:12480820-Mesenteric Arteries, pubmed-meshheading:12480820-Mice, pubmed-meshheading:12480820-Mice, Inbred C57BL, pubmed-meshheading:12480820-Mice, Inbred mdx, pubmed-meshheading:12480820-Microcirculation, pubmed-meshheading:12480820-Muscle Tonus, pubmed-meshheading:12480820-Nitric Oxide Synthase, pubmed-meshheading:12480820-Nitric Oxide Synthase Type II, pubmed-meshheading:12480820-Nitric Oxide Synthase Type III, pubmed-meshheading:12480820-Splanchnic Circulation, pubmed-meshheading:12480820-Stress, Mechanical, pubmed-meshheading:12480820-Vascular Patency, pubmed-meshheading:12480820-Vascular Resistance, pubmed-meshheading:12480820-Vasodilation
pubmed:year
2002
pubmed:articleTitle
Defect in microvascular adaptation to chronic changes in blood flow in mice lacking the gene encoding for dystrophin.
pubmed:affiliation
Institut National de la Santé et de la Recherche Médicale Unit 541, IFR Circulation-Paris-Nord, Paris VII University, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't