Linked Life Data

8401952

Source:http://linkedlifedata.com/resource/pubmed/id/8401952

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1993-11-2
pubmed:abstractText
1. The effects of bacterial lipopolysaccharide (Escherichia coli 0111-B4; LPS) on coronary vascular tone were examined in the isolated perfused heart of the rat. The role of nitric oxide and/or prostaglandin products of the cyclo-oxygenase pathway in mediating the actions of LPS were also investigated. 2. Coronary vascular tone was raised and maintained by a continuous perfusion of the thromboxane-mimetic U46619 (5 nM). LPS perfusion (0.1-100 micrograms ml-1) caused a concentration-dependent fall in coronary tone without any significant change in the force of cardiac contractility. 3. At 5 micrograms ml-1, LPS reduced perfusion pressure by 38 +/- 9 mmHg. This effect was rapid in onset, maximal within the first 5 min and sustained for 90 +/- 10 min (n = 6). 4. The vasodilatation induced by LPS was dependent on the presence of an intact endothelium and abolished following endothelial damage caused by air embolism. 5. NG-nitro-L-arginine methylester (L-NAME; 50 microM) or NG-nitro-L-arginine (L-NOARG; 50 microM) blocked the vasodilatation induced by LPS (5 micrograms ml-1). The inhibition caused by these arginine analogues was partially reversed by 1 mM L- but not D-arginine. 6. The vasodilator action of LPS was also completely blocked by the glucocorticoid, dexamethasone (10 microM) but unaffected by indomethacin (10 microM). 7. These results suggest that LPS evokes rapid release of nitric oxide (NO) in the microvasculature of the rat isolated heart presumably via activation of the constitutive L-arginine-NO pathway in the endothelium. Furthermore, the lack of effect of indomethacin suggests that prostaglandins released via the cyclo-oxygenase pathway are not involved in mediating this action of LPS.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1293292, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1516112, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1657268, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1692936, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1700903, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1701990, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1702214, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1706208, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1723917, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-1852778, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2155799, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2169727, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2181441, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2226626, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2244897, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2282451, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2328404, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2402244, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2473308, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2497467, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2719705, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2790378, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-2924084, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-3110273, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-3131684, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-3265919, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-3390182, http://linkedlifedata.com/resource/pubmed/commentcorrection/8401952-6756397
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
109
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
987-91
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:8401952-15-Hydroxy-11 alpha,9..., pubmed-meshheading:8401952-Animals, pubmed-meshheading:8401952-Arginine, pubmed-meshheading:8401952-Blood Pressure, pubmed-meshheading:8401952-Coronary Circulation, pubmed-meshheading:8401952-Cyclooxygenase Inhibitors, pubmed-meshheading:8401952-Dexamethasone, pubmed-meshheading:8401952-Endothelium, Vascular, pubmed-meshheading:8401952-Escherichia coli, pubmed-meshheading:8401952-Heart, pubmed-meshheading:8401952-Indomethacin, pubmed-meshheading:8401952-Lipopolysaccharides, pubmed-meshheading:8401952-Male, pubmed-meshheading:8401952-Microcirculation, pubmed-meshheading:8401952-NG-Nitroarginine Methyl Ester, pubmed-meshheading:8401952-Nitric Oxide, pubmed-meshheading:8401952-Nitroarginine, pubmed-meshheading:8401952-Perfusion, pubmed-meshheading:8401952-Prostaglandin Endoperoxides, Synthetic, pubmed-meshheading:8401952-Rats, pubmed-meshheading:8401952-Rats, Sprague-Dawley, pubmed-meshheading:8401952-Vasoconstrictor Agents, pubmed-meshheading:8401952-Vasodilation
pubmed:year
1993
pubmed:articleTitle
Bacterial endotoxin rapidly stimulates prolonged endothelium-dependent vasodilatation in the rat isolated perfused heart.
pubmed:affiliation
Vascular Biology Research Centre, King's College, London.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't