Expression of Bcl-2 and bax in the frontoparietal cortex of the rat following cardiac arrest

Following 10-min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. This phenomenon peaked at 14 days and disappeared by 45 days after cardiac arrest. The mechanisms for the initial dysfunction and later restoration of motor function are not completely known. In the present study, involvement of Bcl-2 and Bax in these phenomena was investigated. In the frontoparietal cortex, both bcl-2 and bax mRNA levels were significantly increased 1, 3, 7, 14, and 28 days postresuscitation. bax mRNA levels continued to be high 45 days postcardiac arrest, whereas bcl-2 mRNA levels were returned to control levels. The apoptotic cells were found in layers IV to VI of the frontoparietal cortex of rats 3 days postcardiac arrest. These results indicate that after cardiac arrest, the initial rise of Bax levels may mediate apoptosis and neurodegeneration in the rat brain. At later time points, increased levels of Bcl-2 may contribute to recovery of motor function in posthypoxic rats.