Neurological injury develops over days following cardiac arrest (CA); however, the exact mechanisms remain unknown. After stroke or trauma, the progression of neurological injury is associated with cortical-spreading depolarizations (CSDs). The objective was to investigate whether CA and subsequent resuscitation in rats are associated with 1) the development of spontaneous negative direct current (DC) shifts indicative of CSDs, and 2) changes in artificially induced CSDs in the postresuscitation period. Male Sprague-Dawley rats were randomized into four groups: 1) CA 90, 2) Control 90, 3) CA 360, and 4) Control 360. Following 8 min of asphyxial CA, animals were resuscitated using adrenaline, ventilation, and chest compressions. Animals were observed for 90 or 360 min, respectively, before a 210-min data collection period. Cortical potentials were recorded through burr holes over the right hemisphere. Animals were intubated and monitored with invasive blood pressure, ECG, and arterial blood gas samples throughout the study. Spontaneous DC shifts occurred in only 1 of the 14 CA animals. In control animals, DC shifts were easy to induce, and their shape was highly uniform, consistent with that of classical CSDs. In CA animals, significantly fewer DC shifts could be induced, and their shape was profoundly altered compared with controls. We observed frequent epileptiform discharges and temporal clusters of activity. Spontaneous CSDs were not a consistent finding in CA animals. Instead, spontaneous epileptiform discharges and temporal cluster of activity were observed, while the shapes of induced DC shifts were profoundly altered compared with controls. © 2017 Wiley Periodicals, Inc.
Keywords: direct current; epileptiform discharge; hypoxia; ischemia-reperfusion; temporal cluster.
© 2017 Wiley Periodicals, Inc.