Oxygen and glucose deprivation-induced neuronal apoptosis is attenuated byhalothane and isoflurane

Both in vitro and in vivo evidence supports the reduction of early ischemic , both global and focal, brain injury by volatile anesthetics. However, the protection afforded by volatile anesthetics in later neuronal death, i.e., apoptosis, caused by global ischemia has not been investigated. We induced oxygen and glucose deprivation in neuronal cortical cell cultures prepared from newborn rats on in vitro Days 10-14. This hypoxic (Po-2 < 50 mm Hg) c ondition was maintained continuously (30, 60, and 90 min). In a separate ex periment, the neuronal cell cultures were exposed to isoflurane (1.13%, 2.3 %, or 3.3%) or halothane (1.7%,3.4%, or 5.1%) before oxygen and glucose dep rivation, with continued exposure to isoflurane or halothane during oxygen and glucose deprivation. After 48 h, neuronal apoptosis was assessed with t erminal deoxynucleotidyl transferase-mediated in situ nick-end labeling and DNA gel electrophoresis. Oxygen and glucose deprivation (30, 60, and 90 mi n) caused significant apoptosis of cerebral cortical cultured neurons. Howe ver, pretreatment and continued treatment during the period of oxygen and g lucose deprivation with halothane or isoflurane resulted in a concentration -dependent attenuation of oxygen and glucose deprivation-induced neuronal a poptosis.