Document Detail


Merits of non-invasive rat models of left ventricular heart failure.
MedLine Citation:
PMID:  21279739     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Heart failure (HF) is characterized as a limitation to cardiac output that prevents the heart from supplying tissues with adequate oxygen and predisposes individuals to pulmonary edema. Impaired cardiac function is secondary to either decreased contractility reducing ejection (systolic failure), diminished ventricular compliance preventing filling (diastolic failure), or both. To study HF etiology, many different techniques have been developed to elicit this condition in experimental animals, with varying degrees of success. Among rats, surgically induced HF models are the most prevalent, but they bear several shortcomings, including high mortality rates and limited recapitulation of the pathophysiology, etiology, and progression of human HF. Alternatively, a number of non-invasive HF induction methods avoid many of these pitfalls, and their merits in technical simplicity, reliability, survivability, and comparability to the pathophysiologic and pathogenic characteristics of HF are reviewed herein. In particular, this review focuses on the primary pathogenic mechanisms common to genetic strains (spontaneously hypertensive and spontaneously hypertensive heart failure), pharmacological models of toxic cardiomyopathy (doxorubicin and isoproterenol), and dietary salt models, all of which have been shown to induce left ventricular HF in the rat. Additional non-invasive techniques that may potentially enable the development of new HF models are also discussed.
Authors:
Alex P Carll; Monte S Willis; Robert M Lust; Daniel L Costa; Aimen K Farraj
Related Documents :
8862939 - The value of nifedipine in the treatment of hypertension, coronary heart disease and my...
10526939 - Dissociation of vascular tolerance and plasma norepinephrine adjustment during long-ter...
16352049 - Coffee and coronary heart disease.
1649699 - Endogenous plasma na,k-atpase inhibitory activity and digoxin like immunoreactivity aft...
3092969 - Course of angina pectoris after an acute coronary event.
1835559 - A new strategy for the reduction of acute myocardial infarction in variant angina.
14603369 - Discharge patterns of preganglionic neurones with axons in a cardiac vagal branch in th...
7137149 - Contrasting patterns of familiality for cholesterol and triglyceride in finland accordi...
12208379 - Dissociation of hospitalization and mortality trends for myocardial infarction in the u...
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Cardiovascular toxicology     Volume:  11     ISSN:  1559-0259     ISO Abbreviation:  Cardiovasc. Toxicol.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-03     Completed Date:  2012-03-07     Revised Date:  2014-04-15    
Medline Journal Info:
Nlm Unique ID:  101135818     Medline TA:  Cardiovasc Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  91-112     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Disease Models, Animal*
Heart Failure / genetics,  physiopathology*
Humans
Hypertension / complications,  genetics,  physiopathology
Rats
Rats, Inbred SHR
Sodium, Dietary / adverse effects
Ventricular Dysfunction, Left / genetics,  physiopathology*
Grant Support
ID/Acronym/Agency:
R01 HL104129/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Sodium, Dietary

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


Previous Document:  Family quality of life in dementia: a qualitative approach to family-identified care priorities.
Next Document:  The Role of Aldosterone in the Metabolic Syndrome.