Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
1998-3-11
|
| pubmed:abstractText |
The aim of the current study was to determine if the effects of muscarinic stimulation on left ventricular function and metabolism are greater during beta-adrenergic activation, whether a cyclic GMP-mediated mechanism is responsible, and if this is altered by left ventricular hypertrophy (LVH) induced by aortic valve stenosis. Acetylcholine (Ach) (5 micrograms/kg/min) and/or isoproterenol (Iso) (0.1 micrograms/kg/min) was infused into a branch of the left anterior descending (LAD) artery in 8 control and 8 LVH open-chest anesthetized dogs. LVH increased heart weight, heart-to-body weight ratio and systolic left ventricular pressure. LVH reduced muscarinic receptor density (fmol/mg protein) (control: 149.2+/-18.6; LVH: 77.8+/-8.6), but not affinity. Alone, Ach had no effect on regional force, work or metabolism. Iso increased peak force (g) (control: baseline-7.4+/-0.4; Iso-12.4+/-2.2; LVH: baseline-6.7+/-0.8; Iso-16.3+/-2.7, regional work (g mm/min)) (control: baseline-1250+/-186; Iso-1813+/-409; LVH: baseline-927+/-235; Iso-1244+/-222), and O2 consumption (ml O2/min/100 g) (control: baseline-3.3+/-0.2; Iso-8.1+/-2.0; LVH: baseline-4.8+/-1.0; Iso-8.3+/-1.1). During Iso, Ach reduced segment shortening (control: Iso-14.5+/-1.2; Iso+Ach-10.5+/-1.8; LVH: Iso-10.4+/-1.5; Iso+Ach-7.6+/-1.3) and peak force (control: Iso+Ach-7.7+/-1.0; LVH: Iso+Ach-10.5+/-1.4). Ach also reduced work (control: Iso+Ach-875+/-217; LVH: Iso+Ach-776+/-180) and O2 consumption (control: Iso+Ach-3.4+/-0.7; LVH: Iso+Ach-3.6+/-0.6) in the presence of Iso. Cyclic GMP was higher in the LVH animals during all treatments and was elevated from baseline by Ach in both groups. Neither Iso nor Iso+Ach had a significant effect on cyclic GMP. Thus, the negative functional and metabolic effects of muscarinic stimulation are enhanced during beta-adrenergic activation. This does not, however, appear to be dependent on a cyclic GMP-mediated mechanism. Despite reduced number of muscarinic receptors, this response was not altered by pressure-induced cardiac hypertrophy.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0300-8428
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
92
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
391-401
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9464863-Animals,
pubmed-meshheading:9464863-Cardiomegaly,
pubmed-meshheading:9464863-Cyclic GMP,
pubmed-meshheading:9464863-Dogs,
pubmed-meshheading:9464863-Hypertrophy, Left Ventricular,
pubmed-meshheading:9464863-Receptors, Adrenergic, beta,
pubmed-meshheading:9464863-Receptors, Muscarinic
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
The negative functional and metabolic effects of muscarinic stimulation are enhanced by beta-adrenergic activation in control and hypertrophic dog hearts in vivo.
|
| pubmed:affiliation |
UMDNJ-Robert Wood Johnson Medical School, Department of Surgery, New Brunswick, New Jersey 08903-0019, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|