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Updated: Jun 10, 2026
Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy
Published on: April 17, 2020
Introducing a mouse model of brain death
G Pomper1, K Trescher, D Santer
1Ludwig Boltzmann Cluster for Cardiovascular Research, C/O Core Unit for Biomedical Research, Medical University of Vienna, Vienna General Hospital, Währinger Gürtel 18-20, 1090 Vienna, Austria. gabriela.pomper@meduniwien.ac.at
Experimental animal models of brain death increasing intracranial pressure (ICP) by inflating an intracranial placed balloon-catheter are well established and used in transplant-associated studies. Our aim was to develop an experimental mouse model of brain death (BD) and to compare explosive and gradual brain death induction under ICP monitoring. We therefore induced BD in female OF-1 mice by injecting 40 microl saline every 5 min into an intracranial placed balloon increasing ICP rapidly [BD ex, n=7], or gradually [BD grad, n=7] with 20 microl volume every 5 min under electroencephalogram (EEG) and ICP monitoring until BD occurred. The major criterion for BD was a flat-line-EEG, confirmed by cessation of spontaneous respiration and maximally dilated and fixed pupils. ICP, central activity and heart rate were continuously monitored during the entire 6h follow-up. In sham-operated controls [control, n=7] a burr hole was drilled but no balloon inserted. The BD groups showed equal ICP levels at the time of BD. Both groups had increased heart rates (HR) 15 min after BD, HR decreased to 402+/-29.39 bpm (beats per minute) [BD ex] and 409.33+/-26.46 bpm [BD grad] (n.s. vs. control) by 30 min after the inflation of the balloon, but only BD ex showed a significant decrease in HR compared to control, progressively decreasing thereafter. On the basis of these results, we conclude that the mouse model of brain death can be performed in a standardized, reproducible and successful way.
Experimental animal models of brain death increasing intracranial pressure (ICP) by inflating an intracranial placed balloon-catheter are well established and used in transplant-associated studies. Our aim was to develop an experimental mouse model of brain death (BD) and to compare explosive and gradual brain death induction under ICP monitoring. We therefore induced BD in female OF-1 mice by injecting 40 microl saline every 5 min into an intracranial placed balloon increasing ICP rapidly [BD ex, n=7], or gradually [BD grad, n=7] with 20 microl volume every 5 min under electroencephalogram (EEG) and ICP monitoring until BD occurred. The major criterion for BD was a flat-line-EEG, confirmed by cessation of spontaneous respiration and maximally dilated and fixed pupils. ICP, central activity and heart rate were continuously monitored during the entire 6h follow-up. In sham-operated controls [control, n=7] a burr hole was drilled but no balloon inserted. The BD groups showed equal ICP levels at the time of BD. Both groups had increased heart rates (HR) 15 min after BD, HR decreased to 402+/-29.39 bpm (beats per minute) [BD ex] and 409.33+/-26.46 bpm [BD grad] (n.s. vs. control) by 30 min after the inflation of the balloon, but only BD ex showed a significant decrease in HR compared to control, progressively decreasing thereafter. On the basis of these results, we conclude that the mouse model of brain death can be performed in a standardized, reproducible and successful way.
