Document Detail


Chronic amlodipine treatment during the development of heart failure.
MedLine Citation:
PMID:  9778333     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: This study examined the effects of chronic amlodipine treatment on left ventricular (LV) pump function, systemic hemodynamics, neurohormonal status, and regional blood flow distribution in an animal model of congestive heart failure (CHF) both at rest and with treadmill exercise. In an additional series of in vitro studies, LV myocyte contractile function was examined. METHODS AND RESULTS: Sixteen pigs were studied under normal control conditions and after the development of chronic pacing-induced CHF (240 bpm, 3 weeks, n=8) or chronic pacing and amlodipine (1.5 mg . kg-1 . d-1, n=8). Under ambient resting conditions, LV stroke volume (mL) was reduced with CHF compared with the normal control state (16+/-2 versus 31+/-2, P<0.05) and increased with concomitant amlodipine treatment (29+/-2, P<0.05). At rest, systemic and pulmonary vascular resistance (dyne . s-1 . cm-5) increased with CHF compared with the normal control state (3102+/-251 versus 2156+/-66 and 1066+/-140 versus 253+/-24, respectively, both P<0.05) and were reduced with amlodipine treatment (2108+/-199 and 480+/-74, respectively, P<0.05). With CHF, LV stroke volume remained reduced and was associated with a 40% reduction in myocardial blood flow during treadmill exercise, whereas chronic amlodipine treatment normalized LV stroke volume and improved myocardial blood flow. Resting and exercise-induced plasma norepinephrine levels were increased by >5-fold in the CHF group and were reduced by 50% from CHF values with chronic amlodipine treatment. Resting plasma endothelin (fmol/mL) increased with CHF compared with the normal state (10.4+/-0.9 versus 3.1+/-0.3, P<0.05) and was reduced with amlodipine treatment (6.6+/-1.1, P<0.5). With CHF, LV myocyte velocity of shortening ( microm/s) was reduced compared with normal controls (39+/-1 versus 64+/-1, P<0.05) and was increased with chronic amlodipine treatment (52+/-1, P<0.05). CONCLUSIONS: Chronic amlodipine treatment in this model of developing CHF produced favorable hemodynamic, neurohormonal, and contractile effects in the setting of developing CHF.
Authors:
F G Spinale; R Mukherjee; R S Krombach; M J Clair; J W Hendrick; W V Houck; L Hebbar; S B Kribbs; J L Zellner; M G Dodd
Related Documents :
16025053 - Effect of treatment by laser-assisted uvulopalatoplasty on cardiopulmonary exercise tes...
8370193 - Changes in pulmonary hemodynamics predict benefits in exercise capacity after ace inhib...
11078263 - Correlation of myocardial doppler velocity response to exercise with independent eviden...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  98     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1998 Oct 
Date Detail:
Created Date:  1998-11-05     Completed Date:  1998-11-05     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1666-74     Citation Subset:  AIM; IM    
Affiliation:
Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Amlodipine / therapeutic use*
Animals
Coronary Circulation / drug effects
Exercise Test
Heart Failure / prevention & control*
Hemodynamics / drug effects*
Hormones / secretion
Myocardial Contraction / drug effects
Swine
Time Factors
Vasodilator Agents / therapeutic use*
Ventricular Dysfunction, Left / drug therapy*
Grant Support
ID/Acronym/Agency:
HL-45024/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Hormones; 0/Vasodilator Agents; 88150-42-9/Amlodipine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Apoptosis and cell proliferation after porcine coronary angioplasty.
Next Document:  Development of endothelium-dependent relaxation in canine coronary collateral arteries.