Beard Daniel J, McLeod Damian D, Logan Caitlin L, Murtha Lucy A, Imtiaz Mohammad S, van Helden Dirk F, Spratt Neil J
School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia.
1] School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, New South Wales, Australia [2] Computational Cardiology Laboratory, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia.
J Cereb Blood Flow Metab. 2015 May;35(5):861-72. doi: 10.1038/jcbfm.2015.2. Epub 2015 Feb 11.
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.
近期的人体影像学研究表明，尽管动脉闭塞稳定，但通过软脑膜侧支血管的血流减少（“侧支循环衰竭”）与晚期梗死灶扩大有关。“侧支循环衰竭”的原因尚不清楚。我们最近发现，即使是轻微的实验性中风后24小时，颅内压（ICP）也会急剧但短暂地升高。我们推测颅内压升高会减少侧支血流。首先，我们研究了中风再灌注期间通过侧支血管及其发出的穿通小动脉的血流调节。将Wistar大鼠进行大脑中动脉（MCA）腔内闭塞（MCAo）。使用荧光微球对单个软脑膜侧支和相关穿通小动脉的血流进行定量。MCAo后，基线双向血流立即转变为向MCA方向的血流，并增加了>450%。侧支直径变化极小。其次，我们确定了颅内压升高对侧支和分水岭穿通小动脉血流的影响。在MCAo期间逐步人工升高颅内压。颅内压升高与侧支和穿通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由侧支血管两端的压力降驱动，而非血管直径。颅内压升高会降低脑灌注压和侧支血流，这可能是进行性中风中“侧支循环衰竭”的原因。
