Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1985-5-20
pubmed:abstractText
Milrinone increases left ventricular (LV) shortening. Whether these changes result from vasodilation alone or from a combination of vasodilation and a positive inotropic action is controversial. Load-independent end-systolic indexes of LV contractility were measured over a wide range of aortic pressures generated by methoxamine infusion before and during milrinone administration. Sixteen studies were performed using echocardiography and calibrated carotid pulse tracings in 11 normal subjects. Milrinone loading doses of 30, 45 or 60 micrograms/kg were given intravenously over 10 minutes, followed by a maintenance infusion to achieve steady-state drug levels. Milrinone induced a dose-dependent decrease in baseline (i.e., before methoxamine) total systemic resistance (p less than 0.05) and afterload as measured by end-systolic wall stress (p less than 0.001). The associated changes in the end-systolic pressure-dimension, stress-shortening and stress-velocity of fiber shortening relations were characteristic of a positive inotropic intervention. All end-systolic indexes of LV contractility demonstrated greater inotropic effect at the higher milrinone plasma concentrations. Thus, load-independent indexes of LV contractility show that milrinone has a dose-related positive inotropic effect separate from its vasodilator (total systemic resistance) and afterload (end-systolic stress) reducing effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0002-9149
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1204-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
Physiologic assessment of the inotropic, vasodilator and afterload reducing effects of milrinone in subjects without cardiac disease.
pubmed:publicationType
Journal Article