Global and regional differences in cerebral blood flow after asphyxial versus ventricular fibrillation cardiac arrest in rats using ASL-MRI

RESUSCITATION

卷:85

Article

Drabek, Tomas^1,2  Foley, Lesley M.³  Janata, Andreas¹  Stezoski, Jason^1,2  Hitchens, T. Kevin³  Manole, Mioara D.^1,4  Kochanek, Patrick M.^1,5 

[1] Univ Pittsburgh, Safar Ctr Resuscitat Res, Pittsburgh, PA 15260 USA

[2] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA 15260 USA

[3] Carnegie Mellon Univ, Pittsburgh NMR Ctr Biomed Res, Pittsburgh, PA 15213 USA

[4] Univ Pittsburgh, Dept Pediat, Pittsburgh, PA 15260 USA

[5] Univ Pittsburgh, Dept Crit Care Med, Pittsburgh, PA 15260 USA

关键词: Cardiac arrest;    Resuscitation;    Cerebral blood flow;    Magnetic resonance imaging;    Brain;   

DOI  :  10.1016/j.resuscitation.2014.03.314

来源: Elsevier

【 摘 要 】

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 8 min 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 1 h 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 7 min RT (RT7; 199% vs. BL, Baseline, in cortex and 201% in thalamus, p < 0.05), then returning close to BL at similar to RT15. In contrast, VFCA model induced mild hyperemia, peaking at RT7 (141% vs. BL in cortex). Both ACA and VFCA showed delayed hypoperfusion (ACA, similar to 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. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

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