Transition to collateral flow after arterial occlusion predisposes to cerebral venous steal.
Transition to collateral flow after arterial occlusion predisposes to cerebral venous steal.
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DOI:
10.1161/strokeaha.111.635037
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发表时间:
2012-02
期刊:
影响因子:
8.3
通讯作者:
Liebeskind DS
中科院分区:
文献类型:
--
作者:
Pranevicius O;Pranevicius M;Pranevicius H;Liebeskind DS
Stroke related tissue pressure increase in the core (Pcore) and penumbra (Ppen) determines regional cerebral perfusion pressure (rCPP) defined as a difference between local inflow pressure (Pi) and venous (Pv) or tissue pressure, whichever is higher. We previously showed that venous pressure reduction below the Pcore causes blood flow diversion - cerebral venous steal. Now we investigated how transition to collateral circulation after complete arterial occlusion affects rCPP distribution. We modified two parallel Starling resistor model to simulate transition to collateral inflow after complete main stem occlusion. We decreased Pv from the arterial pressure (Pa) to zero, and investigated how arterial and venous pressure elevation augments rCPP. When core pressure exceeded venous (Pcore>Pv), rCPP=Pi−Pcore. Venous pressure (Pv) decrease from Pa to Pcore caused smaller Pi to drop augmenting rCPP. Further drop of Pv to Ppen decreased rCPP in the core but augmented rCPP in penumbra. After transition to collateral circulation, lowering Pv below Ppen further decreased rCPP and collaterals themselves became pathway for steal. Venous pressure level at which rCPP in the core becomes zero we termed the “point of no reflow” (PONR). Transition from direct to collateral circulation resulted in decreased Pi, decreased rCPP, and a shift of PONR to higher venous loading values. Arterial pressure augmentation increased rCPP, but only after venous pressure exceeded PONR. 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.