Document Detail


The origin of vasovagal syncope: to protect the heart or to escape predation?
MedLine Citation:
PMID:  18592129     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Major lines of evidence suggest that classical (emotional and orthostatic) vasovagal syncope (VVS) is not a disease, but rather a manifestation of a non-pathological trait. It is, therefore, reasonable to investigate the possible factors that may explain its origin and evolution. We reviewed the data available in the literature on the vasovagal reaction in humans and animals in order to identify possible similarities that might provide insight into the evolution of VVS. We found two processes which appear relevant to the investigation of VVS evolution: fear and threat bradycardia in animals, and the vasovagal reflex during hemorrhagic shock in humans and animals. We suggest that VVS in humans involves physiological mechanisms similar to those found in other vertebrates, and that this may indicate a common evolutionary root. The available data seem to suggest that VVS evolved as an advantageous response to inescapable predators or to stressful and possibly dangerous heart conditions. The inhibition of the sympathetic system, together with activation of the vagal system, characterizes VVS. The consequent slowing of the heart rate induced by VVS may constitute a beneficial break of the cardiac pump, thereby reducing myocardial oxygen consumption. We suggest that classical VVS did not evolve recently in the modern human lineage; rather, it should be regarded as a selected response, which probably evolved in the ancient past as a "defense mechanism" of the organism within some ancestral group(s) of vertebrates.
Authors:
Paolo Alboni; Marco Alboni; Giorgio Bertorelle
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Publication Detail:
Type:  Journal Article; Review     Date:  2008-06-30
Journal Detail:
Title:  Clinical autonomic research : official journal of the Clinical Autonomic Research Society     Volume:  18     ISSN:  0959-9851     ISO Abbreviation:  Clin. Auton. Res.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-08-12     Completed Date:  2008-10-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9106549     Medline TA:  Clin Auton Res     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  170-8     Citation Subset:  IM    
Affiliation:
Division of Cardiology, Ospedale Civile, 44042, Cento, FE, Italy. p.alboni@ausl.fe.it
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure
Bradycardia / physiopathology*
Evolution
Fear
Heart Rate
Humans
Reflex
Shock, Hemorrhagic / physiopathology*
Syncope, Vasovagal / etiology,  physiopathology*

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


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