The Acute Phase of Experimental Subarachnoid Hemorrhage: Intracranial Pressure Dynamics and Their Effect on Cerebral Blood Flow and Autoregulation
The Acute Phase of Experimental Subarachnoid Hemorrhage: Intracranial Pressure Dynamics and Their Effect on Cerebral Blood Flow and Autoregulation
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DOI：
10.1007/s12975-018-0674-3
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发表时间：
2019-10-01
影响因子：
6.9
通讯作者：
Schubert, Gerrit A.
中科院分区：
文献类型：
--
作者：
Conzen, Catharina;Becker, Katrin;Schubert, Gerrit A.
蛛网膜下腔出血（SAH）的临床表现和神经系统结局差异很大。动脉瘤性SAH（aSAH）的特点是颅内压（ICP）突然升高和急性灌注不足，导致早期脑损伤（EBI）和预后不良，而具有相当血量的轻度或非动脉瘤性SAH与较好的神经预后相关，可能是由于ICP变化不太明显。因此，急性压力动力学可能是决定神经系统并发症和结果的重要病理生理学方面。我们通过在SAH实验模型中调节注射速度和成分，研究了颅内压变异性对SAH后急性变化的影响。脑池内注射500 μ l动脉血（AB）或生理盐水（NS），持续1（AB（1），NS 1），10（AB（10，NS 10）或30 min（AB（30）），监测6 h（n = 68）。快速血液注射导致最高的ICP峰值（AB（1）中位数142.7 mmHg [1.Q 116.7-3.Q 230.6]，AB（30）33.42 mmHg [18.8-38.3]，p < 0.001）和最严重的低灌注（AB（1）16.6% [11.3-30.6]，AB（30）44.2% [34.8-59.8]; P < 0.05）。然而，30分钟后，所有血型均显示出相当的ICP升高和长期低灌注。除NS 10组外，所有组的脑自动调节最初均因ICP立即升高而中断;然而，只有AB（1）导致自动调节持续受损以及早期神经元细胞丢失。出血的速度和成分导致了特征性的超急性血流动力学变化，尽管ICP范围不同，但灌注不足的情况相当。只有快速ICP增加与明显和早期，但持续的脑自动调节中断，可能有助于EBI。
Clinical presentation and neurological outcome in subarachnoid hemorrhage (SAH) is highly variable. Aneurysmal SAH (aSAH) is hallmarked by sudden increase of intracranial pressure (ICP) and acute hypoperfusion contributing to early brain injury (EBI) and worse outcome, while milder or non-aneurysmal SAH with comparable amount of blood are associated with better neurological outcome, possibly due to less dramatic changes in ICP. Acute pressure dynamics may therefore be an important pathophysiological aspect determining neurological complications and outcome. We investigated the influence of ICP variability on acute changes after SAH by modulating injection velocity and composition in an experimental model of SAH. Five hundred microliters of arterial blood (AB) or normal saline (NS) were injected intracisternally over 1 (AB(1), NS1), 10 (AB(10,) NS10), or 30 min (AB(30)) with monitoring for 6 h (n = 68). Rapid blood injection resulted in highest ICP peaks (AB(1) median 142.7 mmHg [1.Q 116.7-3.Q 230.6], AB(30) 33.42 mmHg [18.8-38.3], p < 0.001) and most severe hypoperfusion (AB(1) 16.6% [11.3-30.6], AB(30) 44.2% [34.8-59.8]; p < 0.05). However, after 30 min, all blood groups showed comparable ICP elevation and prolonged hypoperfusion. Cerebral autoregulation was disrupted initially due to the immediate ICP increase in all groups except NS10; only AB(1), however, resulted in sustained impairment of autoregulation, as well as early neuronal cell loss. Rapidity and composition of hemorrhage resulted in characteristic hyperacute hemodynamic changes, with comparable hypoperfusion despite different ICP ranges. Only rapid ICP increase was associated with pronounced and early, but sustained disruption of cerebral autoregulation, possibly contributing to EBI.