Document Detail


Transition to collateral flow after arterial occlusion predisposes to cerebral venous steal.
MedLine Citation:
PMID:  22246692     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND PURPOSE: Stroke-related tissue pressure increase in the core and penumbra determines regional cerebral perfusion pressure (rCPP) defined as a difference between local inflow pressure and venous or tissue pressure, whichever is higher. We previously showed that venous pressure reduction below the pressure in the core causes blood flow diversion-cerebral venous steal. Now we investigated how transition to collateral circulation after complete arterial occlusion affects rCPP distribution.
METHODS: We modified parallel Starling resistor model to simulate transition to collateral inflow after complete main stem occlusion. We decreased venous pressure from the arterial pressure to zero and investigated how arterial and venous pressure elevation augments rCPP.
RESULTS: When core pressure exceeded venous, rCPP=inflow pressure in the core. Venous pressure decrease from arterial pressure to pressure in the core caused smaller inflow pressure to drop augmenting rCPP. Further drop of venous pressure decreased rCPP in the core but augmented rCPP in penumbra. After transition to collateral circulation, lowering venous pressure below pressure in the penumbra further decreased rCPP and collaterals themselves became a pathway for steal. Venous pressure level at which rCPP in the core becomes zero we termed the "point of no reflow." Transition from direct to collateral circulation resulted in decreased inflow pressure, decreased rCPP, and a shift of point of no reflow to higher venous loading values. Arterial pressure augmentation increased rCPP, but only after venous pressure exceeded point of no reflow.
CONCLUSIONS: In the presence of tissue pressure gradients, transition to collateral flow predisposes to venous steal (collateral failure), which may be reversed by venous pressure augmentation.
Authors:
Osvaldas Pranevicius; Mindaugas Pranevicius; Henrikas Pranevicius; David S Liebeskind
Publication Detail:
Type:  Journal Article     Date:  2012-01-12
Journal Detail:
Title:  Stroke; a journal of cerebral circulation     Volume:  43     ISSN:  1524-4628     ISO Abbreviation:  Stroke     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-24     Completed Date:  2012-08-15     Revised Date:  2014-09-08    
Medline Journal Info:
Nlm Unique ID:  0235266     Medline TA:  Stroke     Country:  United States    
Other Details:
Languages:  eng     Pagination:  575-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Arterial Occlusive Diseases / complications,  physiopathology*
Blood Pressure / physiology
Central Venous Pressure / physiology
Cerebral Arteries / physiopathology
Cerebral Veins / physiopathology
Cerebrovascular Disorders / etiology,  physiopathology*
Collateral Circulation / physiology*
Humans
Models, Anatomic
Stroke / physiopathology
Grant Support
ID/Acronym/Agency:
K23 NS054084/NS/NINDS NIH HHS; K23 NS054084-05/NS/NINDS NIH HHS; K24 NS072272/NS/NINDS NIH HHS; K24 NS072272-01A1/NS/NINDS NIH HHS
Comments/Corrections

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


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