Cardiac Arrest in Rodents: Maximal Duration Compatible with a Recovery of Neuronal Activity

• Published in: Proceedings of the National Academy of Sciences - PNAS 1998-04, Vol.95 (8), p.4748-4753
• Main Authors: Charpak, S., Audinat, E.
• Format: Article
• Language: English
• Subjects: Animals; Bicuculline - pharmacology; Biological Sciences; Body tissues; Brain; Brain - physiology; Brain - physiopathology; Cardiac arrest; Critical periods; Excitatory Amino Acid Antagonists - pharmacology; Excitatory Postsynaptic Potentials - drug effects; Gene Expression Regulation; Genes, fos; Heart Arrest - physiopathology; Heart attacks; In Vitro Techniques; Membrane Potentials - drug effects; Messenger RNA; Neurology; Neurons; Neurons - physiology; Neuroscience; Olfactory pathways; Organ Specificity; Overdose; Polymerase Chain Reaction; Proto-Oncogene Proteins c-fos - biosynthesis; Pyramidal cells; Pyramidal Cells - physiology; Quinoxalines - pharmacology; Rats; RNA, Messenger - biosynthesis; Rodents; Synapses - physiology; Transcription, Genetic
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.95.8.4748

We report here that during a permanent cardiac arrest, rodent brain tissue is ``physiologically'' preserved in situ in a particular quiescent state. This state is characterized by the absence of electrical activity and by a critical period of 5-6 hr during which brain tissue can be reactivated upon restoration of a simple energy (glucose/oxygen) supply. In rat brain slices prepared 1-6 hr after cardiac arrest and maintained in vitro for several hours, cells with normal morphological features, intrinsic membrane properties, and spontaneous synaptic activity were recorded from various brain regions. In addition to functional membrane channels, these neurons expressed mRNA, as revealed by single-cell reverse transcription-PCR, and could synthesize proteins de novo. Slices prepared after longer delays did not recover. In a guinea pig isolated whole-brain preparation that was cannulated and perfused with oxygenated saline 1-2 hr after cardiac arrest, cell activity and functional long-range synaptic connections could be restored although the electroencephalogram remained isoelectric. Perfusion of the isolated brain with the γ -aminobutyric acid A receptor antagonist picrotoxin, however, could induce self-sustained temporal lobe epilepsy. Thus, in rodents, the duration of cardiac arrest compatible with a short-term recovery of neuronal activity is much longer than previously expected. The analysis of the parameters that regulate this duration may bring new insights into the prevention of postischemic damages.