title: Transition to collateral flow after arterial occlusion predisposes to cerebral venous steal.
abstract: OBJECTIVE
  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.affiliation: Department of Anesthesiology, New York Hospital Queens, Flushing, NY, USA. opranevicius@aol.com
authors.forename: Osvaldas
authors.initials: O
authors.lastname: Pranevicius
authors.forename: Mindaugas
authors.initials: M
authors.lastname: Pranevicius
authors.forename: Henrikas
authors.initials: H
authors.lastname: Pranevicius
authors.forename: David S
authors.initials: DS
authors.lastname: Liebeskind
mesh_terms: D001157:Arterial Occlusive Diseases / Q000150:complications / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology; D002496:Central Venous Pressure / Q000502:physiology; D002536:Cerebral Arteries / Q000503:physiopathology; D002550:Cerebral Veins / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000503:physiopathology*; D003097:Collateral Circulation / Q000502:physiology*; D006801:Humans; D008953:Models, Anatomic; D020521:Stroke / Q000503:physiopathology