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
Liebeskind DS
中科院分区:
医学1区
文献类型:
--
作者:
Pranevicius O;Pranevicius M;Pranevicius H;Liebeskind DS

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核心(Pcore)和半暗带(Ppen)中卒中相关的组织压力增加决定了局部脑灌注压(rCPP),其定义为局部流入压(Pi)与静脉压(Pv)或组织压(以较高者为准)之间的差值。我们以前表明,低于Pcore的静脉压降低会导致血流转向-脑静脉盗血。现在,我们研究了完全动脉闭塞后过渡到侧支循环如何影响rCPP分布。我们修改了两个平行Starling阻力模型,以模拟完全主干闭塞后向侧支流入的过渡。我们将Pv从动脉压(Pa)降至零,并研究了动脉压和静脉压升高如何增加rCPP。当核心压超过静脉压(Pcore>Pv)时,rCPP=Pi−Pcore。静脉压(Pv)从Pa降低到Pcore导致较小的Pi下降,增加rCPP。进一步降低Pv至Ppen可降低核心区的rCPP,但增加半影区的rCPP。在过渡到侧支循环后,将Pv降低到Ppen以下进一步降低了rCPP,侧支循环本身成为盗血的途径。我们称核心区rCPP为零时的静脉压水平为“无复流点”(PONR)。从直接循环到侧支循环的转变导致Pi降低,rCPP降低,PONR向更高静脉负荷值转变。动脉压升高增加rCPP,但仅在静脉压超过PONR后。在存在组织压差的情况下,向侧支血流的过渡易发生静脉盗血(侧支衰竭),这可通过静脉压升高逆转。
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.