Objective    To investigate the effect of sodium cyanide (NaCN) intoxication on brain energy metabolism in rats under hypoxia.     Methods    Male SD rats were randomized equally into normal altitude group and high altitude hypoxia group. The animals in the high altitude hypoxia group were pre-exposed in a hypobaric chamber simulating 4 000 m above sea level for 3 d and were injected with 3.6 mg/kg NaCN intraperitoneally. The rats in the normal altitude group were treated in a routine laboratory in Chongqing (308 m above sea level). The rats were sacrificed

then the brains were isolated

striatum and hippocampus were separated on ice at 0

0.5

1.0

2.0

4.0 and 6.0 h after intoxication. Brain water content was tested by measuring the ratio of dry/wet weight. Evans blue (EB) determination was used to understand the permeability of blood vessels in the brain. HPLC was employed to test the contents of adenosine monophosphate (ATP)

adenosine diphosphate (ADP) and adenosine monophosphate (AMP) in hippocampus and corpus striatum of the rat brain.     Results    The brain water was significantly increased in the rats of high altitude hypoxia group by NaCN intoxication

and ATP and ADP contents were significantly decreased in the tissues of hippocampus and corpus striatum either by hypoxia only or by hypoxia and cyanide intoxications

compared with those in the normal altitude group. However

AMP content in the brain tissues was increased by both.     Conclusion    NaCN intoxication under simulated hypoxia can produce energy metabolism turbulence

which may be involved in brain edema formation.