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颅内高压时脑血管自动调节受损的动态脑血管及颅内压反应性评估

Dynamic Cerebrovascular and Intracranial Pressure Reactivity Assessment of Impaired Cerebrovascular Autoregulation in Intracranial Hypertension.

作者信息

Bragin Denis E, Statom Gloria, Nemoto Edwin M

机构信息

Department of Neurosurgery, University of New Mexico, School of Medicine, Albuquerque, NM, 87131, USA.

出版信息

Acta Neurochir Suppl. 2016;122:255-60. doi: 10.1007/978-3-319-22533-3_51.

Abstract

We previously suggested that the discrepancy between a critical cerebral perfusion pressure (CPP) of 30 mmHg, obtained by increasing intracranial pressure (ICP), and 60 mmHg, obtained by decreasing arterial pressure, was due to pathological microvascular shunting at high ICP [1], and that the determination of the critical CPP by the static cerebral blood flow (CBF) autoregulation curve is not valid with intracranial hypertension. Here, we demonstrated that induced dynamic ICP reactivity (iPRx), and cerebrovascular reactivity (CVRx) tests accurately identify the critical CPP in the hypertensive rat brain, which differs from that obtained by the static autoregulation curve. Step changes in CPP from 70 to 50 and 30 mmHg were made by increasing ICP using an artificial cerebrospinal fluid reservoir connected to the cisterna magna. At each CPP, a transient 10-mmHg increase in arterial pressure was induced by bolus intravenous dopamine. iPRx and iCVRx were calculated as ΔICP/Δ mean arterial pressure (MAP) and as ΔCBF/ΔMAP, respectively. The critical CPP at high ICP, obtained by iPRx and iCVRx, is 50 mmHg, where compromised capillary flow, transition of blood flow to nonnutritive microvascular shunts, tissue hypoxia, and brain-blood barrier leakage begin to occur, which is higher than the 30 mmHg determined by static autoregulation.

摘要

我们之前曾提出,通过升高颅内压(ICP)测得的临界脑灌注压(CPP)为30 mmHg,而通过降低动脉压测得的为60 mmHg,二者之间的差异是由于高ICP时病理性微血管分流所致[1],并且在颅内高压情况下,通过静态脑血流量(CBF)自动调节曲线来确定临界CPP是无效的。在此,我们证明,诱导动态ICP反应性(iPRx)和脑血管反应性(CVRx)测试能够准确识别高血压大鼠脑内的临界CPP,这与通过静态自动调节曲线获得的结果不同。通过连接至枕大池的人工脑脊液储液器升高ICP,使CPP从70 mmHg逐步变化至50 mmHg和30 mmHg。在每个CPP水平,通过静脉推注多巴胺诱导动脉压短暂升高10 mmHg。iPRx和iCVRx分别计算为ΔICP/Δ平均动脉压(MAP)和ΔCBF/ΔMAP。通过iPRx和iCVRx在高ICP时测得的临界CPP为50 mmHg,此时毛细血管血流受损、血流向非营养性微血管分流转变、组织缺氧和血脑屏障渗漏开始出现,这一数值高于通过静态自动调节确定的30 mmHg。

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