Linked Life Data

3414494

Source:http://linkedlifedata.com/resource/pubmed/id/3414494

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1988-10-13
pubmed:abstractText
In aortic valvular stenosis, coronary reserve has been shown to be markedly diminished despite normal coronary arteries. To gain further insight into this phenomenon, we examined the effects of an acute subaortic valvular obstruction on coronary blood flow (CBF) in seven open-chest anesthetized dogs. Transient subaortic obstruction was produced by inflating a catheter-tip balloon in the left ventricular (LV) outflow tract. The degree of obstruction, a 26 +/- 3 mm Hg gradient across the aortic valve, was adjusted to achieve an elevation of LV pressure while maintaining a constant aortic pressure (coronary perfusion pressure). In seven dogs with intact coronary vasomotor tone, systolic left anterior descending CBF decreased from 20 +/- 9 ml/min during the control period to 13 +/- 3 ml/min during subaortic obstruction (p less than 0.001). Diastolic CBF increased from 52 +/- 9 to 58 +/- 10 ml/min (p less than 0.05), and total CBF remained unchanged. In three dogs with maximal coronary vasodilation, systolic CBF decreased during subaortic obstruction, diastolic CBF remained unchanged, and total CBF decreased. The present data suggest that elevation of LV intracavitary pressure above coronary perfusion pressure can reduce systolic CBF and lead to an autoregulatory compensation that taxes coronary flow reserve.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0002-8703
pubmed:author
pubmed:issnType
Print
pubmed:volume
116
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
806-11
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Reduction of systolic coronary blood flow in experimental left ventricular outflow tract obstruction.
pubmed:affiliation
Henry Ford Heart and Vascular Institute, Detroit, MI 48202.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't