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Although deep hypothermic circulatory arrest has been known to induce neuronal injury, the molecular mechanism of this damage has not been identified. We studied the key molecular mediators through cellular energy failure, excitotoxicity, and overactivation of poly(adenosine diphosphate-ribose) polymerase 1 in brain tissues of a rabbit model of deep hypothermic circulatory arrest similar to clinical settings.

journal of thoracic and cardiovascular surgery

Overactivation of poly(adenosine phosphate–ribose) polymerase 1 and molecular events in neuronal injury after deep hypothermic circulatory arrest: Study in a rabbit model