It is hypothesized that blood flow is disrupted in brain capillaries after cardiac arrest, contributing to secondary brain injury post-resuscitation, and that targeted pharmacological interventions can improve capillary function and enhance neurological outcomes. The mechanisms and interventions will be investigated using a mouse model of cardiac arrest before translating the findings to a more clinically relevant porcine model.
Secondary brain injury after cardiac arrest – mechanisms and promising therapies
Neurological injury is the foremost cause of disability and death after cardiac arrest, accounting for approximately 60% of all fatalities, and currently no pharmacological therapies are available to prevent such brain injury. Understanding and targeting the mechanisms underlying secondary brain injury after cardiac arrest is the primary focus of the research project
The study aims to explore the mechanisms of brain capillary dysfunction after cardiac arrest and assess whether pharmacological intervention post-resuscitation can prevent this dysfunction and improve neurological outcomes.
The study will use a longitudinal design to assess brain blood flow and injury before and after cardiac arrest. Asphyxial cardiac arrest will be assessed in mice with chronic cranial windows, allowing visualization of capillary blood flow using two-photon microscopy. These findings will then be translated to a more clinically relevant porcine cardiac arrest model, where brain hemodynamics and brain injury will be evaluated using MRI.
Prof. Asger Granfeldt, Department of Anaesthesiology and Intensive Care, Aarhus University Hospital
Eugenio Gutiérrez-Jiménez, Assoc. Prof., Department of Anaesthesiology and Intensive Care, Aarhus University Hospital
Prof. Anna Devor, Department of Bioengineering, Boston University
Prof. Leif Østergaard, Center of Functionally Integrative Neuroscience, Aarhus University