Department of Neurosurgery, University of California Los Angeles, Los Angeles, CA, USA.
Cardiac Arrhythmia Center, Department of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Auton Neurosci. 2022 Sep;241:102987. doi: 10.1016/j.autneu.2022.102987. Epub 2022 May 6.
Cerebral vasospasm is a complex disease resulting in reversible narrowing of blood vessels, stroke, and poor patient outcomes. Sympathetic perivascular nerve fibers originate from the superior cervical ganglion (SCG) to innervate the cerebral vasculature, with activation resulting in vasoconstriction. Sympathetic pathways are thought to be a significant contributor to cerebral vasospasm.
We sought to demonstrate that stimulation of SCG in swine can cause ipsilateral cerebral perfusion deficit similar to that of significant human cerebral vasospasm. Furthermore, we aimed to show that inhibition of SCG can block the effects of sympathetic-mediated cerebral hypoperfusion.
SCG were surgically identified in 15 swine and were electrically stimulated to achieve sympathetic activation. CT perfusion scans were performed to assess for changes in cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT) and time-to-maximum (TMax). Syngo.via software was used to determine regions of interest and quantify perfusion measures.
SCG stimulation resulted in 20-30% reduction in mean ipsilateral CBF compared to its contralateral unaffected side (p < 0.001). Similar results of hypoperfusion were seen with CBV, MTT and TMax with SCG stimulation. Prior injection of lidocaine to SCG inhibited the effects of SCG stimulation and restored perfusion comparable to baseline (p > 0.05).
In swine, SCG stimulation resulted in significant cerebral perfusion deficit, and this was inhibited by prior local anesthetic injection into the SCG. Inhibiting sympathetic activation by targeting the SCG may be an effective treatment for sympathetic mediated cerebral hypoperfusion.
脑血管痉挛是一种复杂的疾病，导致血管可逆性收缩、中风和患者预后不良。交感神经节后纤维起源于颈上交感神经节（SCG），支配脑血管，其激活导致血管收缩。交感神经通路被认为是脑血管痉挛的重要原因。
我们旨在证明刺激猪的 SCG 可以引起类似于人类严重脑血管痉挛的同侧脑灌注不足。此外，我们旨在表明抑制 SCG 可以阻断交感介导的脑低灌注的影响。
在 15 头猪中进行了 SCG 的手术鉴定，并进行电刺激以实现交感神经激活。进行 CT 灌注扫描以评估脑血流（CBF）、脑血容量（CBV）、平均通过时间（MTT）和最大时间（TMax）的变化。使用 Syngo.via 软件确定感兴趣区域并量化灌注测量值。
与对侧未受影响侧相比，SCG 刺激导致平均同侧 CBF 降低 20-30%（p<0.001）。用 SCG 刺激也观察到 CBV、MTT 和 TMax 低灌注的相似结果。预先向 SCG 注射利多卡因抑制了 SCG 刺激的作用，并使灌注恢复到基线水平（p>0.05）。
在猪中，SCG 刺激导致明显的脑灌注不足，而先前向 SCG 注射局部麻醉剂抑制了这种作用。通过靶向 SCG 抑制交感神经激活可能是治疗交感介导脑低灌注的有效方法。
