Document Detail


Factors involved in left ventricular dysfunction after massive sympathetic activation.
MedLine Citation:
PMID:  1415603     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We sought to determine whether catecholamines are responsible for the depressed left ventricular (LV) function that follows massive sympathetic nervous system (SNS) activation and whether the additional myocardial energy demands of SNS-induced hypertension contribute to this disorder. An intracisternal injection of veratrine was used to intensely activate the SNS of anesthetized rabbits, and 150 min later, LV function was evaluated in vitro using established techniques. To assess catecholamine involvement, rabbits were pretreated with phentolamine, propranolol, or saline prior to SNS activation. Control animals received veratrine intravenously. In separate experiments, angiotensin II (ANG II) was administered to rabbits to produce hemodynamic and plasma catecholamine profiles comparable to that produced by intense SNS activity. LV function of hearts after either massive SNS activation or ANG II administration was significantly diminished compared with control (P less than 0.01) and could be prevented by pretreatment with the catecholamine antagonists. LV function was also not diminished in another group of animals in which arterial pressure was maintained near baseline throughout the SNS discharge, thus suggesting that the increased myocardial energy demand associated with the development of arterial hypertension contributes to the LV dysfunction. We conclude that toxic concentrations of catecholamines are responsible for SNS-induced LV dysfunction and that hypertension, most likely because of its ability to increase myocardial energy demand, is one of the important events that leads to depressed cardiac function.
Authors:
C F Pilati; F J Bosso; M B Maron
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  263     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1992 Sep 
Date Detail:
Created Date:  1992-10-29     Completed Date:  1992-10-29     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H784-91     Citation Subset:  IM    
Affiliation:
Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / drug effects,  physiology
Catecholamines / physiology
Female
Heart Conduction System / physiology*
Heart Diseases / physiopathology*
Heart Rate / drug effects
Male
Rabbits
Sympathetic Nervous System / drug effects,  physiology*
Ventricular Function, Left*
Veratrine / pharmacology
Grant Support
ID/Acronym/Agency:
HL-43245/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Catecholamines; 62-59-9/Veratrine

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


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