Resuscitation · 2026
The dynamics of cerebral blood flow and cerebral oedema evaluated by MRI following resuscitation from cardiac arrest; a porcine study.
СтатьяНазвание и аннотация: Перевод в очереди
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Johannsen Cecilie Munch, Lund Margrete Hjuler, Kridal Sebastian, Kjærsgaard Lykke, Hermann Katrine Østergaard, Risager Benjamin Hørning, Svalgaard Anne Drejer, Stæhr Christian, Vammen Lauge, Christensen Nichlas Vous, Szocska Hansen Esben Søvsø, Ringgaard Steffen, Laustsen Christoffer, Andersen Lars, Granfeldt Asger
Аннотация
PURPOSE: To investigate changes in cerebral perfusion and cerebral oedema following cardiac arrest over a 24-h period.
METHOD: Sixteen pigs were randomised to two groups: cardiac arrest group (n = 10) and sham group (n = 6). The cardiac arrest group was subjected to myocardial infarction and 9 min of untreated cardiac arrest. Cerebral blood flow and oedema were evaluated by repeated magnetic resonance imaging (MRI) at 3, 6, 12, and 24 h after achieving return of spontaneous circulation (ROSC). Sham pigs underwent MRI scans at corresponding time points.
RESULTS: Global cerebral blood flow was lower in the cardiac arrest group with a mean group difference of 14.1 mL 100 g-1 min-1 (95% CI: 1.1-27.1; p = 0.028) at 6 h and 15.1 mL 100 g-1 min-1 (95% CI: 1.9-28.3; p = 0.018) at 12 h. Indications of cytotoxic oedema were present at 6 h in the form of lower apparent diffusion coefficient in the cardiac arrest group in the left cortex with a mean difference of 57.8·10-6 mm2/s (95% CI: 12.8-102.8; p = 0.006) and in the right cortex with a mean difference of 64.4 10-6 mm2/s (95% CI: 21.3-107.5; p = 0.001). Neuronal damage was evident by higher neuron specific enolase at 24 h in the cardiac arrest group with a mean difference of -1.14 μg/L (95% CI: -1.77 to -0.50; p < 0.001).
CONCLUSION: We have demonstrated time-dependent cerebral hypoperfusion and region-specific cytotoxic oedema. Our results suggest that cerebral perfusion and cerebral oedema are potential targets of neuroprotection and their development can be evaluated by MRI.
METHOD: Sixteen pigs were randomised to two groups: cardiac arrest group (n = 10) and sham group (n = 6). The cardiac arrest group was subjected to myocardial infarction and 9 min of untreated cardiac arrest. Cerebral blood flow and oedema were evaluated by repeated magnetic resonance imaging (MRI) at 3, 6, 12, and 24 h after achieving return of spontaneous circulation (ROSC). Sham pigs underwent MRI scans at corresponding time points.
RESULTS: Global cerebral blood flow was lower in the cardiac arrest group with a mean group difference of 14.1 mL 100 g-1 min-1 (95% CI: 1.1-27.1; p = 0.028) at 6 h and 15.1 mL 100 g-1 min-1 (95% CI: 1.9-28.3; p = 0.018) at 12 h. Indications of cytotoxic oedema were present at 6 h in the form of lower apparent diffusion coefficient in the cardiac arrest group in the left cortex with a mean difference of 57.8·10-6 mm2/s (95% CI: 12.8-102.8; p = 0.006) and in the right cortex with a mean difference of 64.4 10-6 mm2/s (95% CI: 21.3-107.5; p = 0.001). Neuronal damage was evident by higher neuron specific enolase at 24 h in the cardiac arrest group with a mean difference of -1.14 μg/L (95% CI: -1.77 to -0.50; p < 0.001).
CONCLUSION: We have demonstrated time-dependent cerebral hypoperfusion and region-specific cytotoxic oedema. Our results suggest that cerebral perfusion and cerebral oedema are potential targets of neuroprotection and their development can be evaluated by MRI.