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Updated: Jul 15, 2026
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
Post-cardiac arrest brain injury model: neurobiomarker kinetics following global cerebral hypoperfusion-reperfusion
Ábel Papp1, Levente L Horváth2, Zsófia Nagy3
1Department of Anaesthesiology and Intensive Therapy, Medical School, University of Pécs, Ifjúság str. 13, H-7624 Pécs, Hungary; Hungarian National Ambulance Service, Markó str. 22, H-1055 Budapest, Hungary.
Background:
Post-cardiac arrest brain injury is driven by both global cerebral hypoperfusion and subsequent reperfusion. However, hyperacute blood-based neurobiomarker kinetics after precisely defined (very) low-flow intervals remain poorly characterized. During transcatheter aortic valve implantation (TAVI), rapid ventricular pacing (RVP) induces a transient pulseless ventricular tachycardia, functionally mimicking brief cardiac arrest.
Methods:
In this single-center, prospective, self-controlled cohort study, adults undergoing TAVI were enrolled. RVP (120-200 bpm) was applied to transiently suppress forward flow. Invasive aortic pressure, common carotid (CCA) and middle cerebral artery (MCA) flow were recorded continuously. Serum samples were obtained pre-procedure and 20, 65, 110 and 200 min after RVP. Neuron specific enolase (NSE), and S100 were measured as neurobiomarkers.
Results:
In case of the 76 enrolled patients, median cumulative RVP duration was 60 s (IQR 41-92). During RVP, MCA and CCA flow showed a very low-flow state while aortic pressure fell below the presumed autoregulatory threshold. NSE concentrations increased progressively from baseline to 200 min (T0: 10.6 [9.1-13.0]; T20: 12.8 [11.6-15.5]; T65: 15.1 [13.0-18.6]; T110: 15.8 [13.8-18.6]; T200: 17.0 [14.2-20.5] µg/L). S100B concentrations showed an inverse U-shaped profile (T0: 0.05 [0.04-0.07]; T20: 0.13 [0.10-0.18]; T65: 0.14 [0.11-0.23]; T110: 0.11 [0.08-0.16]; T200: 0.08 [0.06-0.12] µg/L). No patient developed neurological deficits.
Conclusions:
Controlled (very) low-flow episodes during TAVI induce measurable, but clinically silent, elevations of NSE and S100. Neurobiomarkers reflects with distinct kinetics on ischaemia and reperfusion following a short, very low-flow cardiac arrest.
