Drabek Tomas, Foley Lesley M, Janata Andreas, Stezoski Jason, Hitchens T Kevin, Manole Mioara D, Kochanek Patrick M
Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA, United States; Department of Anesthesiology, University of Pittsburgh, Pittsburgh, PA, United States.
Pittsburgh NMR Center for Biomedical Research, Carnegie Mellon University, Pittsburgh, PA, United States.
Resuscitation. 2014 Jul;85(7):964-71. doi: 10.1016/j.resuscitation.2014.03.314. Epub 2014 Apr 12.
Both ventricular fibrillation cardiac arrest (VFCA) and asphyxial cardiac arrest (ACA) are frequent causes of CA. However, only isolated reports compared cerebral blood flow (CBF) reperfusion patterns after different types of CA, and even fewer reports used methods that allow serial and regional assessment of CBF. We hypothesized that the reperfusion patterns of CBF will differ between individual types of experimental CA. In a prospective block-randomized study, fentanyl-anesthetized adult rats were subjected to 8min VFCA or ACA. Rats were then resuscitated with epinephrine, bicarbonate, manual chest compressions and mechanical ventilation. After the return of spontaneous circulation, CBF was then serially assessed via arterial spin-labeling magnetic resonance imaging (ASL-MRI) in cortex, thalamus, hippocampus and amygdala/piriform complex over 1h resuscitation time (RT). Both ACA and VFCA produced significant temporal and regional differences in CBF. All regions in both models showed significant changes over time (p<0.01), with early hyperperfusion and delayed hypoperfusion. ACA resulted in early hyperperfusion in cortex and thalamus (both p<0.05 vs. amygdala/piriform complex). In contrast, VFCA induced early hyperperfusion only in cortex (p<0.05 vs. other regions). Hyperperfusion was prolonged after ACA, peaking at 7min RT (RT7; 199% vs. BL, Baseline, in cortex and 201% in thalamus, p<0.05), then returning close to BL at ∼RT15. In contrast, VFCA model induced mild hyperemia, peaking at RT7 (141% vs. BL in cortex). Both ACA and VFCA showed delayed hypoperfusion (ACA, ∼30% below BL in hippocampus and amygdala/piriform complex, p<0.05; VFCA, 34-41% below BL in hippocampus and amygdala/piriform complex, p<0.05). In conclusion, both ACA and VFCA in adult rats produced significant regional and temporal differences in CBF. In ACA, hyperperfusion was most pronounced in cortex and thalamus. In VFCA, the changes were more modest, with hyperperfusion seen only in cortex. Both insults resulted in delayed hypoperfusion in all regions. Both early hyperperfusion and delayed hypoperfusion may be important therapeutic targets. This study was approved by the University of Pittsburgh IACUC 1008816-1.
心室颤动性心脏骤停（VFCA）和窒息性心脏骤停（ACA）都是心脏骤停（CA）的常见原因。然而，仅有个别报告比较了不同类型心脏骤停后脑血流量（CBF）的再灌注模式，而且使用能够对CBF进行连续和区域评估方法的报告更少。我们推测，不同类型的实验性心脏骤停后CBF的再灌注模式会有所不同。在一项前瞻性分组随机研究中，用芬太尼麻醉的成年大鼠经历了8分钟的VFCA或ACA。然后用肾上腺素、碳酸氢盐、手动胸外按压和机械通气对大鼠进行复苏。自主循环恢复后，在1小时的复苏时间（RT）内，通过动脉自旋标记磁共振成像（ASL-MRI）对皮质、丘脑、海马体和杏仁核/梨状复合体的CBF进行连续评估。ACA和VFCA均在CBF方面产生了显著的时间和区域差异。两个模型中的所有区域随时间均显示出显著变化（p<0.01），表现为早期高灌注和延迟性低灌注。ACA导致皮质和丘脑早期高灌注（与杏仁核/梨状复合体相比，两者p<0.05）。相比之下，VFCA仅在皮质诱导早期高灌注（与其他区域相比，p<0.05）。ACA后高灌注持续时间延长，在复苏时间7分钟（RT7）时达到峰值（皮质为199% vs. 基线，丘脑为201%，p<0.05），然后在约RT15时恢复接近基线水平。相比之下，VFCA模型诱导轻度充血，在RT7时达到峰值（皮质为141% vs. 基线）。ACA和VFCA均显示延迟性低灌注（ACA，海马体和杏仁核/梨状复合体比基线低约30%，p<0.05；VFCA，海马体和杏仁核/梨状复合体比基线低34 - 41%，p<0.05）。总之，成年大鼠的ACA和VFCA在CBF方面均产生了显著的区域和时间差异。在ACA中，皮质和丘脑的高灌注最为明显。在VFCA中，变化较为适度，仅在皮质出现高灌注。两种损伤均导致所有区域延迟性低灌注。早期高灌注和延迟性低灌注都可能是重要的治疗靶点。本研究经匹兹堡大学机构动物护理与使用委员会（IACUC）1008816 - 1批准。
