Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke
Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke
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DOI：
10.1038/jcbfm.2015.2
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发表时间：
2015-05-01
影响因子：
6.3
通讯作者：
Spratt, Neil J.
中科院分区：
文献类型：
--
作者：
Beard, Daniel J.;McLeod, Damian D.;Spratt, Neil J.
最近的人体影像学研究表明，尽管动脉闭塞稳定，但通过枢轴侧支血管的血流量减少（“侧支衰竭”）与晚期梗死扩张有关。“附带失效”的原因尚不清楚。我们最近发现，即使是轻微的实验性脑卒中后24小时，颅内压（ICP）也会急剧升高。我们假设ICP升高会减少侧支血流量。首先，我们研究了卒中再灌注过程中侧支血管和小动脉的血流调节。采用脑腔内大脑中动脉闭塞术（MCAo）治疗Wistar大鼠。用荧光微球定量测定个体头侧支和相关的穿透性小动脉血流。基线双向流量转变为mca定向流量，MCAo后立即增加了450%。侧枝直径变化最小。其次，我们确定了ICP升高对侧支和分水岭穿透性小动脉流量的影响。在MCAo期间，颅内压被人为地逐步升高。ICP升高与侧支和穿透性小动脉血流减少密切相关。中风后侧支血流的变化似乎主要是由侧支血管的压降驱动的，而不是血管直径。颅内压升高可降低脑灌注压和侧支血流，这可能是进展中卒中“侧支衰竭”的原因。
Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.