Abstract
GRAZ-01-17 Introduction: In contrast to necrosis, apoptosis represents a pattern of cell damage associated with an active intracellular death program. Recent data indicate that cardiac arrest (CA) is followed by neuronal apoptosis [1]. The aim of this study was to determine the effects of the inhibition of caspases on neuronal degeneration and outcome following CA. Methods: After approval by the animal care committee, rats were subjected to CA as described previously [1]. After restoration of spontaneous circulation (ROSC), intracerebroventricular (i.c.v.) injections were carried out in the following groups: Group 1. Z-DEVD-FMK (caspase inhibitor; 2.25 μg × 2) i.c.v. 0.5 h and 24 h after CA; Group 2. Z-FA-FMK (control drug; 2.25 μg × 2) i.c.v. 0.5 h and 24 h after CA; Group 3. Z-DEVD-FMK (60 ng/h) i.c.v. continuously 7 days after CA; Group 4. cerebrospinal fluid i.c.v. continuously 7 days after CA. 7 days after ROSC coronal sections of the brain at the dorsal hippocampal level were taken and stained with cresyl violet and the TUNEL technique. Viable and TUNEL positive neurons were counted in the hippocampal CA1 sector. At 24 h, 3 days, and 7 days after ROSC, animals were tested according to a neurological deficit score (NDS). All experiments were performed in a randomized and blinded setting. Results: At day 7, neuronal degeneration with condensed chromatin in TUNEL + neurons was observed in all groups in the hippocampal CA1 sector. There were no differences regarding the number of viable and TUNEL+ neurons, and the NDS. Conclusions: The detection of TUNEL+ neurons with condensed chromatin suggests an apoptosis-associated pattern of neuronal degeneration. Inhibition of caspases with Z-DEVD-FMK did not show any positive effect on neuronal degeneration and outcome in rats. The present data suggest that neuronal apoptosis after CA is not solely caused by the activation of caspases.
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