Cardiopulmonary bypass and neurologic dysfunction – Results from animal models

Neurologic deficits following cardiac surgery persist as common complications with a significant impact to the patient’s quality of life [1,2]. Clinical manifestations of these deficits are variable, ranging from frank stroke as worst case scenario to the more subtle neurocognitive deficits [2,3]. Despite extensive research in the field, the mechanisms leading to neurologic dysfunctions are not fully understood and neuroprotective drugs or strategies have limited effects. To further elucidate the etiology of cerebral injury following cardiac surgery an appropriate non-clinical disease model is needed. Such a disease model is also required to screen potential neuroprotective drugs in a preclinical environment with regard to safety concerns and effectiveness.