Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.
Critical cerebral perfusion pressure at high intracranial pressure measured by induced cerebrovascular and intracranial pressure reactivity.
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通过诱导的脑血管和颅内压反应性测量的高颅内压下的临界脑灌注压力。
DOI：
10.1097/ccm.0000000000000655
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发表时间：
2014-12
影响因子：
8.8
通讯作者：
Nemoto EM
中科院分区：
文献类型：
--
作者：
Bragin DE;Statom GL;Yonas H;Dai X;Nemoto EM
脑血流自动调节的下限是脑血流开始下降的临界脑灌注压。重要的是，脑灌注压应维持在该水平以上，以确保足够的脑血流，特别是在高颅内压患者中。然而，通过降低平均动脉压获得的50 mm Hg的临界脑灌注压与通过增加颅内压获得的30 mm Hg的值不同，我们先前表明这是由于微血管分流维持假性高脑血流量。目前的研究表明，通过增加颅内压来降低脑灌注压来测量临界脑灌注压是不准确的，但通过多巴胺诱导的动态颅内压反应性和脑血管反应性来准确地确定。比较颅内压升高或平均动脉压降低均能降低脑灌注压，降低临界脑灌注压。在整个研究过程中监测皮质多普勒流量、颅内压和平均动脉压。在每个脑灌注压，我们测量微血管红细胞流速，血脑屏障的完整性（跨毛细血管染料外渗），和组织氧合（减少烟酰胺腺嘌呤二核苷酸）在大鼠大脑皮层使用体内双光子激光扫描显微镜。大学实验室。雄性Sprague-Dawley大鼠在每个脑灌注压下，使用多巴胺诱导的动脉压瞬变（~10 mm Hg，~45 s持续时间）测量诱导的颅内压反应性（Δ颅内压/Δ平均动脉压）和诱导的脑血管反应性（Δ脑血流量/Δ平均动脉压）。在70 mm Hg的正常脑灌注压下，10 mm Hg平均动脉压脉冲对颅内压或脑血流量没有影响（诱导的颅内压反应性= -0.03 ± 0.07，诱导的脑血管反应性= -0.02 ± 0.09），反映了完整的自动调节。通过增加颅内压将脑灌注压降低至50 mm Hg，诱导的颅内压反应性和诱导的脑血管反应性分别增加至0.24 ± 0.09和0.31 ± 0.13，反映了自身调节受损（p < 0.05）。在静态脑血流量下，脑血流量在脑灌注压为30 mm Hg时首次显著降低（0.71 ± 0.08，p < 0.05）。通过诱导颅内压反应性和诱导脑血管反应性准确确定临界脑灌注压为50 mm Hg，而静态方法失败。(Crit Care Med 2014; 42：2582-2590）
The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. University laboratory. Male Sprague-Dawley rats. At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (Δ intracranial pressure/Δ mean arterial pressure) and induced cerebrovascular reactivity (Δ cerebral blood flow/Δ mean arterial pressure). At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = –0.03 ± 0.07 and induced cerebrovascular reactivity = –0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed. (Crit Care Med 2014; 42:2582–2590)