Department of Neurology, University of California, Irvine, Irvine, CA, USA.
Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA, USA.
Neurocrit Care. 2022 Jun;37(Suppl 1):139-154. doi: 10.1007/s12028-022-01530-2. Epub 2022 Jun 21.
Spreading depolarizations (SDs) are self-propagating waves of neuronal and glial depolarizations often seen in neurological conditions in both humans and animal models. Because SD is thought to worsen neurological injury, the role of SD in a variety of cerebral insults has garnered significant investigation. Anoxic SD is a type of SD that occurs because of anoxia or asphyxia. Although asphyxia leading to a severe drop in blood pressure may affect cerebral hemodynamics and is widely known to cause anoxic SD, the effect of anoxic SD on peripheral blood pressure in the extremities has not been investigated. This relationship is especially important to understand for conditions such as circulatory shock and cardiac arrest that directly affect both peripheral and cerebral perfusion in addition to producing anoxic SD in the brain.
In this study, we used a rat model of asphyxial cardiac arrest to investigate the role of anoxic SD on cerebral hemodynamics and metabolism, peripheral blood pressure, and the relationship between these variables in 8- to 12-week-old male rats. We incorporated a multimodal monitoring platform measuring cortical direct current simultaneously with optical imaging.
We found that during anoxic SD, there is decoupling of peripheral blood pressure from cerebral blood flow and metabolism. We also observed that anoxic SD may modify cerebrovascular resistance. Furthermore, shorter time difference between anoxic SDs measured at different locations in the same rat was associated with better neurological outcome on the basis of the recovery of electrocorticography activity (bursting) immediately post resuscitation and the neurological deficit scale score 24 h post resuscitation.
To our knowledge, this is the first study to quantify the relationship between peripheral blood pressure, cerebral hemodynamics and metabolism, and neurological outcome in anoxic SD. These results indicate that the characteristics of SD may not be limited to cerebral hemodynamics and metabolism but rather may also encompass changes in peripheral blood flow, possibly through a brain-heart connection, providing new insights into the role of anoxic SD in global ischemia and recovery.
扩布性去极化(SD)是神经元和神经胶质去极化的自传播波,在人类和动物模型的多种神经状况中经常出现。由于 SD 被认为会加重神经损伤,因此 SD 在各种脑损伤中的作用已经引起了广泛的研究。缺氧性 SD 是由于缺氧或窒息引起的一种 SD 类型。尽管导致严重血压下降的窒息可能会影响脑血流动力学,并且众所周知会引起缺氧性 SD,但缺氧性 SD 对四肢外周血压的影响尚未得到研究。对于循环休克和心脏骤停等直接影响外周和脑灌注并在脑内产生缺氧性 SD 的情况,了解这种关系尤为重要。
在这项研究中,我们使用窒息性心脏骤停大鼠模型来研究缺氧性 SD 对脑血流动力学和代谢、外周血压以及这些变量之间关系的影响,实验对象为 8-12 周龄雄性大鼠。我们结合了一种多模态监测平台,同时测量皮质直流和光学成像。
我们发现,在缺氧性 SD 期间,外周血压与脑血流和代谢脱耦。我们还观察到,缺氧性 SD 可能会改变脑血管阻力。此外,在同一只大鼠的不同部位测量的缺氧性 SD 之间的时间差越短,基于复苏后即刻电皮质图活动(爆发)的恢复和复苏后 24 小时的神经缺陷评分,神经功能恢复越好。
据我们所知,这是第一项定量研究缺氧性 SD 中外周血压、脑血流和代谢与神经功能恢复之间关系的研究。这些结果表明,SD 的特征可能不仅限于脑血流动力学和代谢,还可能包括外周血流的变化,可能通过脑心连接,为缺氧性 SD 在全身缺血和恢复中的作用提供了新的见解。