Document Detail

Functional and morphological characteristics of compensated and decompensated cardiac hypertrophy in dogs with chronic infrarenal aorto-caval fistulas.
MedLine Citation:
PMID:  2137729     Owner:  NLM     Status:  MEDLINE    
The relation between cardiac hypertrophy, shunt size, myocardial contractility, capillary density, adrenergic responsiveness, and neurohumoral stimulation was evaluated in dogs with compensated and decompensated cardiac hypertrophy caused by an infrarenal aorto-caval shunt. Shunt size varied from 5 to 35 mm2 due to an inability to create a uniform size. Dogs that developed heart failure within 4 months had 25 +/- 2 mm2 shunts, whereas those that developed it after 4 months had 19 +/- 3 mm2 shunts; those that did not develop heart failure had 10 +/- 1 mm2 shunts. Hypertrophy developed at the same rate in all the dogs that developed heart failure, which occurred at a critical heart weight (hypertrophy) for a given load (shunt size). In the dogs with heart failure there was a decrease in myocardial contractility (tension = 5.7 +/- 0.6 vs. 7.3 +/- 0.3 g/mm2, p less than 0.05), a decrease in adrenergic responsiveness (maximal heart rate with isoproterenol = 203 +/- 7 vs. 249 +/- 5 beats/min, p less than 0.01), an increase in circulating neurohormones, and a decrease in urinary sodium excretion (0.4 +/- 0.1 vs. 5.0 +/- 1.3 meq/3 hr, p less than 0.01). None of these abnormalities occurred in dogs with compensated hypertrophy. There were no differences in cardiac capillary density between the control dogs and the dogs with compensated cardiac hypertrophy or heart failure. Thus, it would appear that if heart failure is to develop after an initial toleration of a sudden volume overload, it will develop at a given combination of cardiac hypertrophy and volume overload, with cardiac hypertrophy developing at the same rate in all cases. In this model, once heart failure develops, myocardial contractility and cardiac adrenergic responsiveness are decreased and there is pronounced neurohumoral activation. All these changes are absent in hearts with compensated hypertrophy.
F Legault; J L Rouleau; C Juneau; C Rose; K Rakusan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation research     Volume:  66     ISSN:  0009-7330     ISO Abbreviation:  Circ. Res.     Publication Date:  1990 Mar 
Date Detail:
Created Date:  1990-04-06     Completed Date:  1990-04-06     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  846-59     Citation Subset:  IM; S    
Research Center, Hôpital du Sacré-Coeur de Montréal, Université de Montréal, Canada.
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MeSH Terms
Adaptation, Physiological*
Aorta / surgery*
Arteriovenous Shunt, Surgical*
Capillaries / pathology
Cardiac Output, Low / etiology
Cardiomegaly / etiology,  pathology,  physiopathology*
Drug Resistance
Isoproterenol / pharmacology
Papillary Muscles / physiopathology
Physical Exertion
Venae Cavae / surgery*
Water / pharmacology
Reg. No./Substance:
7683-59-2/Isoproterenol; 7732-18-5/Water

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

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