Linked Life Data

3336994

Source:http://linkedlifedata.com/resource/pubmed/id/3336994

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 2
pubmed:dateCreated
1988-2-5
pubmed:abstractText
Cigarette smoking is believed to cause harmful cardiovascular and atherogenic effects resulting from changes in lipid metabolism. Intravenous nicotine and smoking raise plasma free fatty acid (FFA) levels through enhanced lipolysis resulting from sympathoadrenal stimulation. The study reported here investigated FFA-stimulated myocardial oxygen consumption (MVO2) in intact dogs. It was found that about half of the nicotine-induced rise in MVO2 resulted from metabolic stimulation by high concentrations of FFA, and the remainder was a result of enhanced mechanical activity of the heart directly produced by nicotine. In intact dogs, the increase in myocardial oxygen requirement resulting from excess myocardial FFA uptake also increased the severity of myocardial ischemic injury after acute coronary occlusion. Human studies with men who had smoked for more than 10 years showed that smokers had lower plasma high-density lipoprotein cholesterol fractions 2 and 3. High-density lipoprotein fraction 2 is reported to be antiatherogenic. Thus smoking appears to have at least two lipid effects that may promote coronary heart disease and atherosclerosis: increased plasma FFA and decreased plasma high-density lipoprotein cholesterol fraction 2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0002-8703
pubmed:author
pubmed:issnType
Print
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
272-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Lipid effects of smoking.
pubmed:affiliation
Department of Physiology, University of Tromsø, Norway.
pubmed:publicationType
Journal Article