Cerebral Protection by Isoflurane during Hypoxemia or Ischemia

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Abstract
The cerebral metabolic effects of isoflurane suggest that it may provide a degree of cerebral protection similar to that demonstrated for barbiturates. The possible cerebral protecion afforded by isoflurane against hypoxemia and ischemia was studied in mice and dogs, respectively. In mice breathing 5% O2 survival time was increased significantly over control in groups exposed to 1.0 and 1.4% isoflurane. At higher concentrations (2.0 and 3.0%) it is presumed that cardiorespiratory depression contributed to shorter survival times. In 6 dogs the effects of 3% isoflurane on the rates of cerebral ATP and phosphocreatine [PCa] depletion and lactate accumulation during incomplete global ischemia were compared with 6 control dogs exposed to N2O. Incomplete global ischemia was produced by acute hemorrhagic hypotension to 30 mmHg for 9 min, a situation that does not abolishcortical electrical activity (active eEG). In the dogs exposed to isoflurane, the cerebral energy stores of ATP and PCr and the cerebral energy charge were sustained at significantly higher levels than in dogs exposed to N2O, and the cerebral lactate accumulation was significantly less in the initial 7 min of hypotension. Evidently in the circumstances of O2 deprivation insufficient to abolish cortical electrical activity, isoflurane, like the barbiturates, can provide some cerebral protection presumably by depressing cortical electrical activity and cerebral metabolism.

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