title: Possible control of intermittent cerebral ischemia by monitoring of direct-current potentials.
abstract: OBJECTIVE
  Neurosurgically induced temporary occlusion of intracranial arteries carries the risk of cerebral ischemic damage. Because negative shifts in the cortical direct-current (DC) potential indicate tissue depolarization and, thus, critical ischemic stress, the authors hypothesized that recordings of these potentials could help to determine the optimal duration and frequency of induced intermittent focal ischemia to prevent brain injury. The investigators related the results of DC recordings both to simultaneously recorded decreases in extracellular Ca++ concentration ([Ca++]o), which reflect Ca++ entry into cells, and to histological outcome.
  
  
  METHODS
  In cats anesthetized with halothane the effects of intermittent brief (10 minutes long, six times [6 x 10-min group]) and prolonged (20 minutes long, three times [3 x 20-min group]) episodes of middle cerebral artery occlusions were compared with those of a single continuous episode (1 x 60-min group). Laser Doppler flow probes and ion-selective microelectrodes were used to measure cerebral blood flow, DC potentials, and [Ca++]o in cortical tissues of ectosylvian gyri. Negative shifts in DC potential were evaluated in the three groups during the entire 60-minute-long period of ischemia and were smallest in the 6 x 10-min group, larger in the 3 x 20-min group, and largest in the 1 x 60-min group. Accordingly, infarct volumes were smallest in the 6 x 10-min group, intermediate in the 3 x 20-min group, and largest in the 1 x 60-min group. Decreases in ischemic [Ca++]o were significantly greater in the 1 x 60-min group than in the two groups in which there were repetitive occlusions, and recovery of [Ca++]o after reperfusion normalized only in the 1 x 60-min group.
  
  
  CONCLUSIONS
  The DC potential may provide a reliable measure to optimize intermittent ischemia and to achieve minimal ischemic brain injury during temporary neurosurgical occlusion of cerebral arteries.
authors.affiliation: Max-Planck-Institut für neurologische Forschung, Cologne, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Sakaki
authors.forename: R
authors.initials: R
authors.lastname: Graf
authors.forename: H
authors.initials: H
authors.lastname: Nozaki
authors.forename: G
authors.initials: G
authors.lastname: Rosner
authors.forename: W D
authors.initials: WD
authors.lastname: Heiss
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D002415:Cats; D002540:Cerebral Cortex / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology; D004569:Electroencephalography / Q000295:instrumentation; D005260:Female; D007431:Intraoperative Complications / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008839:Microelectrodes; D020768:Middle Cerebral Artery / Q000473:pathology / Q000601:surgery; D016343:Monitoring, Intraoperative / Q000295:instrumentation*; D012039:Regional Blood Flow / Q000502:physiology; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology; D012815:Signal Processing, Computer-Assisted / Q000295:instrumentation*; D009435:Synaptic Transmission / Q000502:physiology*
chemical_list: D002118:Calcium