Denis E Bragin， Gloria Statom， Edwin M Nemoto 美国新墨西哥大学医学院
近期，我们使用体内双光子激光显微扫描（2PLSM），通过大鼠顶叶皮层颅骨窗测量颅内压逐渐升高时微血管红细胞流速、组织氧合和血脑屏障完整性。研究显示，通过增加颅内压，将脑灌注压降至50 mm Hg，低流速毛细血管转变为病理性增加的微血管分流（MVS），伴组织缺氧、脑水肿和血脑屏障开放——非营养性MVS血流特征。
脑灌注压50 mm Hg时的MVS血流，通过皮质多普勒探针获得的静态自动调节曲线显示，30 mm Hg时自动调节功能受损。为验证此发现，我们使用人工脑脊液容器连接到小脑延髓池增加颅内压，使脑灌注压产生从70 mm Hg到50、30 mm Hg阶梯变化。
研究显示，高颅内压时测量动态脑血管反应性（CVRx）和颅内压反应性（PRx），脑灌注压临界值为50 mm Hg，微血管分流、脑水肿、组织缺氧和血脑屏障渗漏开始发生。高速MVS血流模仿自动调节功能假性正常，静态脑血流自动调节确定的高颅内压时临界脑灌注压高于30 mm Hg。多巴胺诱导的平均动脉压升高测定的CVRx和PRx显示，脑灌注压处于50 mm Hg时，脑血管自动调节功能失效，对应2PLSM测定的毛细血管向MVS转变。
Recently we used in vivo 2PLSM through a cranial window over the rat parietal cortex to measure changes in microvascular red blood cell flow velocity， tissue oxygenation and blood brain barrier (BBB) integrity during a progressive increase in intracranial pressure (ICP). We showed that reduction of cerebral perfusion pressure (CPP) to 50 mm Hg by increasing intracranial pressure caused a transition from low velocity capillary to pathologically elevated microvascular shunt (MVS) flow. Notably， this transition was accompanied by the development of tissue hypoxia， brain edema and blood brain barrier opening - characterizing non-nutritive MVS flow.
MVS flow occurred at CPP of 50 mm Hg butin contradiction， static autoregulation curves obtained by cortical Doppler probe showed impaired autoregulation at 30 mm Hg. To validate it， step changes in CPP from 70 to 50 and 30 mm Hg were made by increasing ICP with vertical positioning of an artificial cerebrospinal fluid reservoir connected to the cisterna magna.
Our studies show that at high ICP， the critical CPP is 50 mm Hg as shown by measurements of cerebrovascular reactivity (CVRx) and intracranial pressure reactivity (PRx) and where microvascular shunting， brain edema， tissue hypoxia and BBB leakage begin to occur. This critical CPP at high ICP is higher than the 30 mm Hg determined by static CBF autoregulation because high velocity MVS flow mimics falsely preserved autoregulation. Dynamic CVRx and PRx by dopamine-induced MAP challenge revealed a failure in cerebrovascular autoregulation during intracranial hypertension at a CPP of 50 mm Hg which corresponds to a transition from capillary to MVS flow as measured by 2PLSM.